Guest guest Posted March 1, 2005 Report Share Posted March 1, 2005 Tish, You argue that doses below 3 to 5 grains can make someone even more hypothyroid because lower dose therapy causes the thyroid to lower its production by the dosage amount or more. However, what if the person doesn't have any thyroid production of their own, such as with thyroid gland destroyed by RAI or someone with congenital malformation of the thyroid gland? In those cases, perhaps the TSH would be suppressed with some amount of supplementation, but since the thyroid is already at zero or near production, the person would benefit from even small amounts of thyroid therapy. Could you share your source with me for your statement that the healthy human thyroid makes about 3 to 5 grains a day? When I upped to 3 grains for a couple weeks, I felt like I was a balloon about to burst, and I could feel my blood pulsing in my neck. Even at back down to 2 grains I eventually experienced palpitations. My experience doesn't jive with the idea that we need at least 3 grains a day. Lynn ____________________________________________________________________________ _________________ " lkwetter " wrote on Tuesday, March 01, 2005 6:05 PM Subject: Re: New Labs > Low dose thyroid therapy doesn't work. Studies have found that doses > below 3 to 5 grains do not have any effect on the thyroid status of > people. This is mostly due to the suppressive effect thyroid pills > have on the pituitary (via TSH) which causes the thyroid to lower > it's production by the amount taken or more. You can become even > more hypothyroid on low dose therapy. But, as little as 50 mcg of > Synthroid will suppress TSH into the normal range. So, TSH is no > good for adjusting doses. It is only good for a screening to find > hypothryoidism and even then, about 5% of hypos are missed because > they have secondary hypothyroidism. > > The heatlhy human thyroid makes about 3 to 5 grains a day. In > theory, when you take 1 grain, the pituitary will know this and > adjust TSH to tell the thyroid to make another 2 to 4 grains to get > your daily total up to where you need it or about 3 to 5 grains. > But, in reality it does not work this way and low dose therapy only > causes the pituitary to drop TSH to tell the thyroid to drop thryoid > production by the amount taken or even less. So, the hypo stays > exactly the same and may even get worse. This is what happened to me. > > So, doses have to be high enough to overcome the pituitary > suppression in order to get any changes in the metaboolic rate. > > Tish Quote Link to comment Share on other sites More sharing options...
Guest guest Posted March 1, 2005 Report Share Posted March 1, 2005 I think that what Tish should be saying is that a dose " lower " than what you NEED can cause someone to be even more hypo. I can also see that someone may only " need " 2 grains if their thyroid is not as " sick " or " low producing " as mine. I only seem to need 3 1/4 grains of Armour, but I suspect that 20 years ago, if I had been on Armour, I would have needed less than 3 grains because my thyroid was not as " sick " as it is now. On the other hand, I would think that if a person has NO thyroid, they will NOT do well on a small dose. The BODY needs more than a small dose to perform all it's healthy actions if there is NO thyroid production. Also, you can need less thyroid (whatever that " less " amount is for each individual) when you are doing it sublingually, and spacing it out during the day, than if you were taking it all at once and/or swallowing it. Janie ) > Tish, > > You argue that doses below 3 to 5 grains can make someone even more > hypothyroid because lower dose therapy causes the thyroid to lower its > production by the dosage amount or more. However, what if the person > doesn't have any thyroid production of their own, such as with thyroid gland > destroyed by RAI or someone with congenital malformation of the thyroid > gland? In those cases, perhaps the TSH would be suppressed with some amount > of supplementation, but since the thyroid is already at zero or near > production, the person would benefit from even small amounts of thyroid > therapy. > > Could you share your source with me for your statement that the healthy > human thyroid makes about 3 to 5 grains a day? When I upped to 3 grains for > a couple weeks, I felt like I was a balloon about to burst, and I could > feel my blood pulsing in my neck. Even at back down to 2 grains I > eventually experienced palpitations. My experience doesn't jive with the > idea that we need at least 3 grains a day. > > Lynn > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted March 1, 2005 Report Share Posted March 1, 2005 I think that what Tish should be saying is that a dose " lower " than what you NEED can cause someone to be even more hypo. I can also see that someone may only " need " 2 grains if their thyroid is not as " sick " or " low producing " as mine. I only seem to need 3 1/4 grains of Armour, but I suspect that 20 years ago, if I had been on Armour, I would have needed less than 3 grains because my thyroid was not as " sick " as it is now. On the other hand, I would think that if a person has NO thyroid, they will NOT do well on a small dose. The BODY needs more than a small dose to perform all it's healthy actions if there is NO thyroid production. Also, you can need less thyroid (whatever that " less " amount is for each individual) when you are doing it sublingually, and spacing it out during the day, than if you were taking it all at once and/or swallowing it. Janie ) > Tish, > > You argue that doses below 3 to 5 grains can make someone even more > hypothyroid because lower dose therapy causes the thyroid to lower its > production by the dosage amount or more. However, what if the person > doesn't have any thyroid production of their own, such as with thyroid gland > destroyed by RAI or someone with congenital malformation of the thyroid > gland? In those cases, perhaps the TSH would be suppressed with some amount > of supplementation, but since the thyroid is already at zero or near > production, the person would benefit from even small amounts of thyroid > therapy. > > Could you share your source with me for your statement that the healthy > human thyroid makes about 3 to 5 grains a day? When I upped to 3 grains for > a couple weeks, I felt like I was a balloon about to burst, and I could > feel my blood pulsing in my neck. Even at back down to 2 grains I > eventually experienced palpitations. My experience doesn't jive with the > idea that we need at least 3 grains a day. > > Lynn > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted March 2, 2005 Report Share Posted March 2, 2005 In a message dated 3/2/2005 1:37:21 AM Eastern Standard Time, lmcgaha@... writes: > Could you share your source with me for your statement that the healthy > human thyroid makes about 3 to 5 grains a day? tish will chime in if she hasn't already...but I believe she is citing a older study with desiccated thyroid extract was the only thing in use...as well as other information from then when people took lots more Armour than they do today. Also, there are other thyroid doctors who state the same thing - that person can't go hyper until they go over 4 1/2 - 5 grains. I think the thing to remember here - and as Tish as stated - is that there can be other issues - adrenal, anemia, etc - that can cause problems. I have debated the statement in my mind - on the TSH feedback thing that Tish mentions. I think perhaps we do have to make distinctions between healthy thyroid glands (who will adjust .....although might be depressed for a period of time after withdrawing oral thyroid hormone) and those whose glands are sick. I'm not so sure we can make the same assumptions about the feedback loop working properly when the thyroid gland and/or pituitary may be malfunctioning. Cindi Quote Link to comment Share on other sites More sharing options...
Guest guest Posted March 2, 2005 Report Share Posted March 2, 2005 In a message dated 3/2/2005 1:37:21 AM Eastern Standard Time, lmcgaha@... writes: > Could you share your source with me for your statement that the healthy > human thyroid makes about 3 to 5 grains a day? tish will chime in if she hasn't already...but I believe she is citing a older study with desiccated thyroid extract was the only thing in use...as well as other information from then when people took lots more Armour than they do today. Also, there are other thyroid doctors who state the same thing - that person can't go hyper until they go over 4 1/2 - 5 grains. I think the thing to remember here - and as Tish as stated - is that there can be other issues - adrenal, anemia, etc - that can cause problems. I have debated the statement in my mind - on the TSH feedback thing that Tish mentions. I think perhaps we do have to make distinctions between healthy thyroid glands (who will adjust .....although might be depressed for a period of time after withdrawing oral thyroid hormone) and those whose glands are sick. I'm not so sure we can make the same assumptions about the feedback loop working properly when the thyroid gland and/or pituitary may be malfunctioning. Cindi Quote Link to comment Share on other sites More sharing options...
Guest guest Posted March 2, 2005 Report Share Posted March 2, 2005 In a message dated 3/2/2005 1:37:21 AM Eastern Standard Time, lmcgaha@... writes: > Could you share your source with me for your statement that the healthy > human thyroid makes about 3 to 5 grains a day? tish will chime in if she hasn't already...but I believe she is citing a older study with desiccated thyroid extract was the only thing in use...as well as other information from then when people took lots more Armour than they do today. Also, there are other thyroid doctors who state the same thing - that person can't go hyper until they go over 4 1/2 - 5 grains. I think the thing to remember here - and as Tish as stated - is that there can be other issues - adrenal, anemia, etc - that can cause problems. I have debated the statement in my mind - on the TSH feedback thing that Tish mentions. I think perhaps we do have to make distinctions between healthy thyroid glands (who will adjust .....although might be depressed for a period of time after withdrawing oral thyroid hormone) and those whose glands are sick. I'm not so sure we can make the same assumptions about the feedback loop working properly when the thyroid gland and/or pituitary may be malfunctioning. Cindi Quote Link to comment Share on other sites More sharing options...
Guest guest Posted March 2, 2005 Report Share Posted March 2, 2005 tish, thanks for posting all this great info...i'd printed out some of this before when you posted some items - but great to see it all together...all 18 pages! Cindi Quote Link to comment Share on other sites More sharing options...
Guest guest Posted March 2, 2005 Report Share Posted March 2, 2005 tish, thanks for posting all this great info...i'd printed out some of this before when you posted some items - but great to see it all together...all 18 pages! Cindi Quote Link to comment Share on other sites More sharing options...
Guest guest Posted March 2, 2005 Report Share Posted March 2, 2005 tish, thanks for posting all this great info...i'd printed out some of this before when you posted some items - but great to see it all together...all 18 pages! Cindi Quote Link to comment Share on other sites More sharing options...
Guest guest Posted March 2, 2005 Report Share Posted March 2, 2005 In a message dated 3/2/2005 12:44:52 PM Eastern Standard Time, saltillo@... writes: > I slowly worked on getting my dose up. When > I got to 3 grains, my whole life just became so much better and I > began to finally feel normal Tish, It wasn't unti I got to 3 grains that I started to feel better too. (now at 54 1/2 grains and some Cytomel) And then the doctor wanted to reduce that. That's when i got mad and started self-medicating for months and months until i felt like i was stable and could go to another doctor. I don't think these old sources are wrong. i think they are very right. I think it's good that we know about these old studies when we are using Armour. And i think there are a lot of folks suffering these days because they don't get armour and they don't get enough of it. I will never let a doctor keep me sick again. Cindi Quote Link to comment Share on other sites More sharing options...
Guest guest Posted March 2, 2005 Report Share Posted March 2, 2005 In a message dated 3/2/2005 12:44:52 PM Eastern Standard Time, saltillo@... writes: > I slowly worked on getting my dose up. When > I got to 3 grains, my whole life just became so much better and I > began to finally feel normal Tish, It wasn't unti I got to 3 grains that I started to feel better too. (now at 54 1/2 grains and some Cytomel) And then the doctor wanted to reduce that. That's when i got mad and started self-medicating for months and months until i felt like i was stable and could go to another doctor. I don't think these old sources are wrong. i think they are very right. I think it's good that we know about these old studies when we are using Armour. And i think there are a lot of folks suffering these days because they don't get armour and they don't get enough of it. I will never let a doctor keep me sick again. Cindi Quote Link to comment Share on other sites More sharing options...
Guest guest Posted March 2, 2005 Report Share Posted March 2, 2005 In a message dated 3/2/2005 1:51:26 PM Eastern Standard Time, laurie.brown@... writes: > Uhhh...54 1/2 grains? I think I can see why he wanted to cut you back! > hehe....must have been wishful thinking. try 4 1/2 grains and some cytomel. sometimes 4 grains. the cytomel seems to pick up where the armour leaves off. but i was hypo so long...i doubt my tissues are utilizing and converting the t4 very well. cindi Quote Link to comment Share on other sites More sharing options...
Guest guest Posted March 2, 2005 Report Share Posted March 2, 2005 In a message dated 3/2/2005 1:51:26 PM Eastern Standard Time, laurie.brown@... writes: > Uhhh...54 1/2 grains? I think I can see why he wanted to cut you back! > hehe....must have been wishful thinking. try 4 1/2 grains and some cytomel. sometimes 4 grains. the cytomel seems to pick up where the armour leaves off. but i was hypo so long...i doubt my tissues are utilizing and converting the t4 very well. cindi Quote Link to comment Share on other sites More sharing options...
Guest guest Posted March 2, 2005 Report Share Posted March 2, 2005 In a message dated 3/2/2005 1:51:26 PM Eastern Standard Time, laurie.brown@... writes: > Uhhh...54 1/2 grains? I think I can see why he wanted to cut you back! > hehe....must have been wishful thinking. try 4 1/2 grains and some cytomel. sometimes 4 grains. the cytomel seems to pick up where the armour leaves off. but i was hypo so long...i doubt my tissues are utilizing and converting the t4 very well. cindi Quote Link to comment Share on other sites More sharing options...
Guest guest Posted March 2, 2005 Report Share Posted March 2, 2005 It's my opinion that for the vast majority of hypos, if you have a problem with less than about 3 grains, it's usually a low adrenal issue or an issue with anemia or other nutritional or cellular peoblem where the body cannot use thyroid hormone. This sort of reaction can be from raising your dose too quickly or too much or from being hypo a long time and thus being very sensitive to thyroid hormone. You can easily test for yourself if your dose is adequate by measuring your metabolic rate via body temperature, pulse nad breathing rate: http://www.drrind.com/tempgraph.asp http://www.thyrophoenix.com/self_monitor.htm Studies done with heatlhy people have found that they can tolerate large doses up to 9 grains with no problems. A great way to tell if a person is not hypothyroid is if when given thyroid they experience almost no reaction, either getting better or worse. Hypos are very sensitive to thyroid hormone and dose raises. Circulating thyroid levels control the size and function of the adrenals and control nutritional uptake from the digestive tract. So, the long term hypo person is very compromised in their ability to speed up the metabolic rate with small amounts of thyroid. You are right that Extreemly hypo people or people with destroyed thryoids will get a metabolic increase from low dose therapy. But, that is because they are starting out so low on the scale. But, one study found that leaving people who had thyroidectomy hypothyroid too long seemed to stick them at a low metabolic rate, because when they did give them thyroid at lower doses, their metabolic rates did not increase right away. Here are some of my sources for what I say: ________________________ 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. ________________________ 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. ________________________ 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). _________________ [study of hormone replacement therapy following total thyroidectomy in thyroid cancer--with special reference to the analysis of thyroid hormone peripheral effects, using indirect calorimetry] [Article in Japanese] Nozaki H, Funahashi H, Sato Y, Imai T, Oike E, Kato M, Takagi H. Second Department of Surgery, Nagoya University School of Medicine, Japan. Five weeks after the beginning of hormone replacement, T4 and free T4 were slightly within range, and no enhancement of energy metabolism was noted. From these findings, the post-operative TSH suppression therapy carried out at our department is considered to be justifiable also from the viewpoint of energy metabolism. (This paper points out that they were unabel to raise metabolic rate on thyroidectomized patients unless they suppressed TSH. By not doing so, they were uable to raise the metabolic rate. I believe they used 120mcg of thyroid for this and this did not raise the metabolic rate.) ____________________ http://www.drlowe.com/QandA/askdrlowe/armourthyroid.htm That optimal dosage range is highly individual, but historically, the typical patient's therapeutic window has been somewhere between 120 to 240 mg (2 to 4 grains). There's no way to accurately predict what your therapeutic window is. (Some people can get by on 2 grains, but not very many.) _____________________ Dr. Derry, " Breast Cancer and Iodine " : Before the 1973-1974 change in laboratory diagnosis, the objective of treatment in all cases was raise the thyroid dose up untill the patient was in a state of well-being. Before the 1973-74 change, the normal dose of thyroid was three times the level seen now (2 -3 grains now) and there were no cases of fractures or osteoporosis ever reported in the previous 80 years. ________________________ Broda , " Hypothyroidism, the Unsuspected Illness " Dr. Pericles Menof of South Africa began treatment in his practice with 5 grains of Armour and then reduced if needed. (pg 150) (This caused problems for people with heart problems because starting dose was too high.) In 1925, the smallest starting dosage was 4 grains and dosages up to 30 grains had been used. (page 188) The proper dosage is the minimum to relieve symptoms. ___________________ 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. ______________________________ http://www.drlowe.com/frf/t4replacement/intro.htm The most effective of these therapies involves adjusting patients' dosages of combined T4/T3 or T3 alone according to several indices other than TSH and thyroid hormone levels. Those indices are signs, symptoms, and various objective measures of tissue response to particular dosages. When patients' dosages are titrated according to these indices, dosages that prove safe and effective are typically TSH-suppressive.[44] Evidence is available that this therapeutic approach relieves patients' signs, symptoms, and measurable tissue abnormalities such as low resting metabolic rates (RMR) according to indirect calorimetry. This observation suggests that dosages higher than those dictated by the replacement concept more effectively relieve patients' hypothyroid symptoms. Other research has shown that patients report feeling better with TSH-suppressive dosages of thyroid hormone.[23] [24][25] Moreover, psychiatrists report that dosages of T3 higher than replacement dosages augment the depression-relieving effects of antidepressants.[9][28][29][30][31][34] In addition, in a study of patients made hypothyroid by therapeutic destruction of the thyroid gland, some used TSH-suppressive dosages of thyroid hormone and others used T4-replacement. Those on TSH-suppressive dosages didn't gain excess weight; those on T4-replacement did. The researchers concluded that T4-replacement was the cause of the excess weight gain.[55] These published reports are consistent with thousands of cases in which hypothyroid patients recovered from their symptoms and other health problems with TSH-suppressive dosages of thyroid hormone after T4-replacement failed to help them. Kaplan's observation also suggests another point: that T4- replacement keeps many hypothyroid patients' dosages too low to relieve their symptoms is an indictment of the concept of replacement. As the cause of (1) the continued suffering and debility of patients, (2) an increased incidence of potentially life-threatening diseases, and (3) the need for the chronic use of medications, ___________________________ Dr. Derry article: http://thyroid.about.com/library/derry/bl11.htm The effective dose physicians used by clinical judgment and experience before 1975 was around 2-3 times higher than the dose used by TSH blood test monitoring. So everyone's dose of thyroid after 1975 was decreased by about two thirds of well established clinically effective doses. __________________________ Another Derry article: http://thyroid.about.com/library/derry/bl4a.htm In the 1960s it was textbook material after 70 years of experience using thyroid that a dose below 180 mg of desiccated thyroid (3 grains) could not be measured clinically or in the laboratory. In other words it was without effect.(2) The approximate equivalent dose of synthroid or thyroxine (T4) would be about 180 micrograms. (3) So unless your dose is above 180 there is little chance of regaining your hair back and the problem likely continue and get worse. You can tell when you are approaching the right dose personally when the itching starts to go away permanently. Depending on how old you are and other medical history it is likely though you would get complete relief with a dosage up around 200 micrograms of Synthroid or higher. We know that there are no side effects at those dosages. Dosages of thyroxine (Synthroid, T4) of up to 300 micrograms are without morbidity or mortality. (no sickness or deaths) (4) _____________________________ Dr. Lowe's wife: http://www.drlowe.com/emailnewsletter/2003archive.htm Instead, they adjust dosages according to how patients respond to a particular dose. As studies have shown, this approach produces far superior treatment results than does adjusting dosages according to thyroid test results.[1][2] ___________________________ Dr. Lowe uses this guide: http://www.drlowe.com/clincare/clinicalforms/areyouoverstimulated.pdf to determine if the patient is on too high a dose. In other words, they raise thyroid dose up untill the patient feels best and use this form as a way to make sure they haven't gone too high. Dose is determined purely by how the patient feels and no tests are used _____________________ Author: JAMES C. WREN, M.D. Date Published: 01-Jan-1971 Publication: JOURNAL OF THE AMERICAN GERIATRICS SOCIETY Vol. 19, No 1, p 7, 1971 Title: SYMPTOMATIC ATHEROSCLEROSIS: PREVENTION OR MODIFICATION BY TREATMENT WITH DESICCATED THYROID All patients were given desiccated thyroid in an initial dosage of 15 to 30 mg daily (single dose). This was increased slowly to 60 to 240 mg (4 grains) daily (single dose) within six months, the aim being full replacement or physiological dosage. The final dosage was a matter of clinical judgement rather than laboratory study. In most cases the dosage at six months was maintained throughout the rest of the study. In the majority of cases the daily dosage was 120 mg (104 patients) or 180 mg (190 patients). RESULTS Subjective findings General. In the symptomatic group, 100 of 132 patients reported benefit from thyroid therapy, in the form of an increased sense of well-being, increased exercise tolerance, greater motivation and greater alertness. Twenty-two remained unchanged and 10 died. It is generally conceded that human atherosclerosis is irreversible, but these results indicate that the administration of thyroid may be of benefit in many cases. Probably of most importance and significance was the statistical observation that for these thyroid-treated patients the mortality rate was lower than that for the population at large. (Note the doses. They are quite high on average.) _________________________ Report by by Dr. Hertoghe on his studies of thyroid function Daily production of T4 is about 80 to 100 micrograms and T3 is 20 micrograms. (This is equivelent to 3 grains and does not take into account the amount of thyroid that would be lost to the digestive system by taking pills. It is only measuring actual levels in the blood.) _______________________ email correspondence, January 20, 8:33 am 2005 Dear Leitita Wetterauer, according to the ROCHE medical encyclopedia, the daily turnover of T3 and T4 is 30 and 80 microgramm respectively. I don't have further information, but I think you can find plenty of data in the web. Best regards G. Proehl Dr. Gerhard Proehl GSF-Institute of Radiation Protection Postfach 1129 D-85758 Neuherberg Phone: +49-89-3187-2889 Fax: +49-89-3187-3363 Email: proehl@... (This is equivelent to 200 mcg or just under 3 grains. This does not take into account losses to the digestive system by taking pills.) ______________________ Dr. Guberman http://drguberman.com/news.cfm?date_range=8/01/04 7051 West Commercial Blvd., Suite 3-C Tamarac, FL 33319 e-mail: drguberman@... That optimal dosage range is highly individual, but historically, the typical patient's therapeutic window has been somewhere between 120 to 240 mg (2 to 4 grains). There's no way to accurately predict what your therapeutic window is. Until you find it, you may not improve much from the Armour. But once you do, you're likely to feel that the wait was well worth it. _________________________ Author: P. B. S. Fowler Date Published: 11-Aug-1973 Publication: BMJ 11 August 1973 Vol. III p 352 - 353 Title: LETTER: Treatment of Hypothyroidism this infrequent phenomenon lies in the fact that exogenous thyroid hormone in moderate doses administered to normal subjects rarely has appreciable effects, owing to compensatory suppression of the subject's own thyroid gland through diminished secretion by the pituitary of thyroid-stimulating hormone (TSH). TIns feedback inhibition tends to maintain a constant level of circulating thyroid hormone. There are, in fact, instances of normal subjects who have taken quite appreciably excessive doses of thyroid with minimal or no manifestations of toxicity, probably due to enhanced ability for degradation of excessive 84 amounts of hormone in some individual __________________________ http://www.thyroid-info.com/articles/dommisse.htm An Interview with Dommisse, MD Unique Theories About Hypothyroidism Treatment I ran into too many patients who had classic hypothyroid symptoms, which cleared completely on appropriate thyroid treatment, and whose TSH was below 2.0 (but above 1.5) and with FT4 and FT3 levels in the low ends of their 'normal ranges'….Finally, I found some patients with several symptoms and signs of hypothyroidism whose TSH was between 1.0-1.5; so I lowered my range, for the last time, to 0.1- 1.0; I now treat primary hypothyroidism with a TSH of >1.0 (if the FT4 and FT3 are low-normal, not above the middle of their 'normal ranges'). _______________________ .. " Optimum Diagnosis and Treatment of Hypothyroidism With Free T3 and Free T4 Levels " by Dr. ph Mercola (US), DO http://www.mercola.com/article/hypothyroid/diagnosis_comp.htm Most patients continue to have classic hypothyroid symptoms because excessive reliance is placed on the TSH. This test is a highly accurate measure of TSH but not of the height of thyroid hormone levels. The basic problem that traditional medicine has with diagnosing hypothyroidism is the so called " normal range " of TSH is far too high: Many patients with TSH's of greater than 1.5 (not 4.5) have classic symptoms and signs of hypothyroidism. ______________________ Dr. Derry http://thyroid.about.com/library/derry/bl11.htm Topic: Low Adrenal Function and Thyroid Problems Physicians before 1975 found the minimum clinically effective dose for hypothyroid patients was about 180 mg of desiccated thyroid or 180 micrograms of eltroxine (T4). ____________________ Dr. Derry article: http://thyroid.about.com/library/derry/bl4a.htm In the 1960s it was textbook material after 70 years of experience using thyroid that a dose below 180 mg of desiccated thyroid (3 grains) could not be measured clinically or in the laboratory. In other words it was without effect.(2) The approximate equivalent dose of synthroid or thyroxine (T4) would be about 180 micrograms.(3) So unless your dose is above 180 there is little chance of regaining your hair back and the problem likely continue and get worse. We know that there are no side effects at those dosages. Dosages of thyroxine (Synthroid, T4) of up to 300 micrograms are without morbidity or mortality. (no sickness or deaths) (4) _____________________ Dr. Derry http://www.bites-medical.org/hypo/hist.html (Site now gone) There were no problems with desiccated thyroid even at high doses, and it was known as one of the safest drugs available. Synthetic T4, on the other hand, has had a long history of manufacturing and reliability problems. _____________________ (This paper points out that some patients need suppressive doses of thyroid to feel good.) MINI REVIEW Intrinsic imperfections of endocrine replacement therapy J A Romijn, J WA Smit and S W J Lamberts Department of Endocrinology, Leiden University Medical Center, Leiden and Department of Internal Medicine, Erasmus Medical Center, Rotterdam University, Rotterdam, The Netherlands (Correspondence should be addressed to J A Romijn; Email: j.a.romijn@...) However, many patients treated for endocrine insufficiencies still suffer from more or less vague complaints and a decreased quality of life. It is likely that these complaints are, at least in part, caused by intrinsic imperfections of hormone replacement strategies in mimicking normal hormone secretion. ......effects of hormones in general, and thus of hormone replacement strategies in particular, are difficult to quantify at the tissue level. Therefore, in clinical practice we rely mostly on plasma variables – `plasma endocrinology' – which are a poor reflection of hormone action at the tissue level. Complaints of thyroid patients....They range from musculoskeletal complaints, to vague feelings of being unwell, and to depression. Two approaches have been used to decrease the complaints experienced by these patients: an increase in the dose of L-thyroxine, and combination treatment of thyroxine with tri-iodothyronine. In some of the patients, a decrease in complaints can be achieved by increasing the dose of thyroxine above that required to restore TSH concentrations to normal (1). For this reason, such patients are often allowed to take a dose of thyroxine that would be judged as overtreatment with respect to TSH concentrations. The second approach was evaluated by Bunevicius et al. (2), who performed a randomised controlled trial to compare the effects of thyroxine alone with those of thyroxine plus tri-iodothyronine. Patients with hypothyroidism benefitted when 12.5 mg triiodothyronine was substituted for 50 mg thyroxine in their treatment regimens. This resulted in improved neuropsychological functioning. Pulse rates and serum sex hormone-binding globulin concentrations were greater after treatment with thyroxine plus tri-iodothyronine, indicating a slightly greater effect on the heart and liver. Serum thyroxine concentrations were lower and tri-iodothyronine concentrations were greater after treatment with thyroxine plus tri-iodothyronine, but serum TSH concentrations, a sensitive measure of thyroid hormone action, were similar after the two treatments. It should be noted that not all patients benefitted from this approach because, even in the group with combination therapy, patients continued to report complaints of depression. Thyroxine: The thyroid secretes tri-iodothyronine (T3) (,20%) in addition to thyroxine (T4) (,80%). In the absence of thyroid function, exogenous thyroxine is not able to normalise the concentrations of T4 and T3 in all tissues in rodents, even in the presence of normal TSH concentrations. Despite this knowledge, currently available preparations of T3 have unfavourable pharmacological profiles and adequate markers of biological effect are lacking. Additional evidence is required before combination therapy can be advised. First, it is remarkable that the normal values of TSH show a more than tenfold variation, between 0.4 and 4.5mU/l. Because, in clinical practice, the optimal TSH concentration for individual patients within this range is unknown, titration of the substitution dose of thyroxine within this tenfold variation is relatively crude. Secondly, the intrinsic assumption of many doctors in this approach is that normal TSH concentrations reflect adequate thyroid hormone concentrations, not only at the tissue level of the hypothalamus and the pituitary, but also in the other tissues. However, it is likely that this assumption is erroneous, because TSH is produced only by the pituitary gland and therefore may not reflect thyroid hormone status in tissues outside the hypothalamo– pituitary axis. This notion is supported by data obtained from animal experiments. Thyroxine is considered to be an inactive hormone, because a thyroxine-specific receptor has not been identified. Rather, thyroxine serves as a prohormone, because it is the precursor of tri-iodothyronine. Some tissues, such as muscle, have a relatively low deiodinase activity and are dependent, to a great extent, on tri-iodothyronine derived from the thyroid and the liver. In rodents, it has been clearly demonstrated that there is no single dose of thyroxine or tri-iodothyronine that normalises thyroid hormone concentrations in all tissues simultaneously in hypothyroid animals (3). Therefore, it is highly likely that, in patients treated with L-thyroxine, subtle derangements at the tissue level are present with respect to thyroid hormone availability, and probably also thyroid hormone action. _______________________ Changes in serum triiodothyronine, thyroxine, and thyrotropin during treatment with thyroxine in severe primary hypothyroidism M Maeda, N Kuzuya, Y Masuyama, Y Imai and H Ikeda J. Clin. Endocrinol. Metab., Jul 1976; 43: 10 - 17. It is difficult to assess what is the optimal dose for any one subject, for at present we have no objective, easily quantifiable parameter to assess response of body tissues to thyroid hormone replacement. Measurements of serum TSH, kinetics of reflex time, and oxygen consumption are helpful, but not entirely reliable for this purpose. Individuals on physiological replacement replacement doses of pure sodium levothyroxine have elevated levels (high normal to hyperthyroid range) of serum thyroxine (-Pattee). The resin uptake tests in these persons are also elevated above normal, so that in patients on 300 or 400 pg of sodium levothyroxine (4.0 to 5.5 grains) a day, the PBI or serum thyroxine level will be in the high range and so will the free thyroxine index. (Note the very high doses of Synthroid needed to make the patient feel well. This was before over reliance on the TSH test.) _______________________ (This paper points out that healthy people have little responxe to being given thyroid.) Author: WILLIAM H. BEIERWALTES, M.D. Date Published: 01-Jan-1955 Publication: Michigan Journal Clinical Endocrinology Vol. 15, 1955 p148 - 150 (Editorial) Title: RESPONSE TO THYROID Category: diagnosing Keywords: thyroid, BEIERWALTES, desiccated, oral, research, myxedqamatous, myxoedema, euthyroid , diagnose, basal, pulse rate, iodine Text: 1955 Editorial WILLIAM H. BEIERWALTES, M.D. University Hospital, Ann Arbor, Michigan Journal Clinical Endocrinology Vol. 15, 1955 p148 - 150 p148 RESPONSE TO THYROID WHEN desiccated thyroid is administered orally to myxedematous humans, the resultant metabolic changes are quite different from those observed in the euthyroid subject. The clinician can diagnose or treat hypothyroid patients much more intelligently if he is aware of these difference in response to thyroid. In addition, an unworked field for clinical research becomes evident when one reviews the known major differences between the myxedematous patient and the euthyroid subject in response to desiccated thyroid administration. The most striking difference observed may be summarized by the statement that the patient who is truly deficient in circulating thyroid hormone responds dramatically and with predictable regularity to the administration of small doses of desiccated thyroid. The euthyroid subject, on the other hand, shows no obvious clinical response to small doses of thyroid. A simple and readily available diagnostic test for borderline hypothyroidism, therefore, is the administration of 1 grain of desiccated thyroid per day for a period of six weeks after a careful history and physical examination have been made and basal metabolic rate and serum cholesterol determinations have been performed. The patient who is truly deficient in thyroid hormone will generally respond to the administration of 1 grain of desiccated thyroid per day for six weeks with an increase in basal pulse rate and metabolic rate and a fall in the serum cholesterol level. The patient not truly deficient in thyroid hormone will show no significant change in these indices of thyroid hormone effect. p149 .....The myxedematous patient and the euthyroid subject also show a different response to sudden cessation of desiccated thyroid medication. The myxedematous patient at first shows a rapid drop in his serum precipitable-iodine level and basal metabolic rate, then a slower fall to pre-treatment levels over a period of six to eight weeks (3). On the other hand, when the thyroid medication of a euthyroid person is suddenly stopped, the serum precipitable-iodine value falls to myxedematous levels in three to four weeks, but the basal metabolic rate may take as long as nine to fifteen weeks to reach its lowest level (3). These values then rise to pre-treatment levels. The radioiodine uptake is also falsely depressed by thyroid administration and has taken as long as eleven weeks to recover (4). Furthermore, when the thyroid does recover its ability to concentrate I131, the I131 pickup rate may rebound temporarily to hyperthyroid levels. Obviously, if a physician were to stop the desiccated thyroid medication of a euthyroid patient in an attempt to evaluate the patient's underlying thyroid status, these ensuing changes in indices of thyroid function, when sampled, might prove very misleading and confusing. The daily output of thyroid hormone by the normal thyroid gland is thought to be equivalent to not more than 3 grains of desiccated thyroid per day. Consequently, when the daily dosage of desiccated thyroid is raised to 4 grains or more per day, any differences observed between athyreotic and euthyroid subjects can not be explained on the basis of further suppression of normal thyroid function. Most practicing physicians have probably observed a euthyroid patient who was comfortable while voluntarily taking 5 to 20 grains of desiccated thyroid a day, in an attempt to reduce p149 his weight and rid himself of fatigue. Rarely, if ever, does one see an athyreotic patient voluntarily take more than 3 grains of desiccated thyroid per day. This situation suggests that the athyreotic patient is more sensitive to thyroid substance than is the euthyroid person, even after his myxedema has been controlled with medication. .....WILLIAM H. BEIERWALTES, M.D. University Hospital, Ann Arbor, Michigan REFERENCES 1. MEANS, J. H,: The Thyroid and Its Disease, ed. 2. Philadelphia, J. B. Lippincott Co., 1948, p 249 2. WINKLER, A. W.; RIGGS, D. S., and MAN, E. B.: Serum iodine in hypothyroidism before and during thyroid therapy, J. Clin. Invest. 24: 732, 1945 3. RIGGS, D. S.; MAN, E. B., and WINKLER, A. W.: Serum iodine of euthyroid subjects treated with desiccated thyroid, J. Clin. Invest. 24: 722, 1945 4. GREER, M. A.: The effect on endogenous thyroid activity of feeding desiccated thyroid to normal human subjects, New England J. Med. 244: 385, 1951 5. JOHNSTON, M. W.; SQUIRES, A. H., and FARQHARSON, R. F.: The effect of prolonged administration of thyroid, Ann. Int. Med. 35: 1008, 1951 6. THOMPSON, W. O.; THOMPSON, P. K.; TAYLOR, S. G., and DICKIE, L. F. N.: Calorigenic action of single large doses of desiccated hog thyroid: comparison with the action of thyroxine given orally and intravenously, Arch. Int. Med. 54: 888, 1934 Quote Link to comment Share on other sites More sharing options...
Guest guest Posted March 2, 2005 Report Share Posted March 2, 2005 It's my opinion that for the vast majority of hypos, if you have a problem with less than about 3 grains, it's usually a low adrenal issue or an issue with anemia or other nutritional or cellular peoblem where the body cannot use thyroid hormone. This sort of reaction can be from raising your dose too quickly or too much or from being hypo a long time and thus being very sensitive to thyroid hormone. You can easily test for yourself if your dose is adequate by measuring your metabolic rate via body temperature, pulse nad breathing rate: http://www.drrind.com/tempgraph.asp http://www.thyrophoenix.com/self_monitor.htm Studies done with heatlhy people have found that they can tolerate large doses up to 9 grains with no problems. A great way to tell if a person is not hypothyroid is if when given thyroid they experience almost no reaction, either getting better or worse. Hypos are very sensitive to thyroid hormone and dose raises. Circulating thyroid levels control the size and function of the adrenals and control nutritional uptake from the digestive tract. So, the long term hypo person is very compromised in their ability to speed up the metabolic rate with small amounts of thyroid. You are right that Extreemly hypo people or people with destroyed thryoids will get a metabolic increase from low dose therapy. But, that is because they are starting out so low on the scale. But, one study found that leaving people who had thyroidectomy hypothyroid too long seemed to stick them at a low metabolic rate, because when they did give them thyroid at lower doses, their metabolic rates did not increase right away. Here are some of my sources for what I say: ________________________ 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. ________________________ 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. ________________________ 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). _________________ [study of hormone replacement therapy following total thyroidectomy in thyroid cancer--with special reference to the analysis of thyroid hormone peripheral effects, using indirect calorimetry] [Article in Japanese] Nozaki H, Funahashi H, Sato Y, Imai T, Oike E, Kato M, Takagi H. Second Department of Surgery, Nagoya University School of Medicine, Japan. Five weeks after the beginning of hormone replacement, T4 and free T4 were slightly within range, and no enhancement of energy metabolism was noted. From these findings, the post-operative TSH suppression therapy carried out at our department is considered to be justifiable also from the viewpoint of energy metabolism. (This paper points out that they were unabel to raise metabolic rate on thyroidectomized patients unless they suppressed TSH. By not doing so, they were uable to raise the metabolic rate. I believe they used 120mcg of thyroid for this and this did not raise the metabolic rate.) ____________________ http://www.drlowe.com/QandA/askdrlowe/armourthyroid.htm That optimal dosage range is highly individual, but historically, the typical patient's therapeutic window has been somewhere between 120 to 240 mg (2 to 4 grains). There's no way to accurately predict what your therapeutic window is. (Some people can get by on 2 grains, but not very many.) _____________________ Dr. Derry, " Breast Cancer and Iodine " : Before the 1973-1974 change in laboratory diagnosis, the objective of treatment in all cases was raise the thyroid dose up untill the patient was in a state of well-being. Before the 1973-74 change, the normal dose of thyroid was three times the level seen now (2 -3 grains now) and there were no cases of fractures or osteoporosis ever reported in the previous 80 years. ________________________ Broda , " Hypothyroidism, the Unsuspected Illness " Dr. Pericles Menof of South Africa began treatment in his practice with 5 grains of Armour and then reduced if needed. (pg 150) (This caused problems for people with heart problems because starting dose was too high.) In 1925, the smallest starting dosage was 4 grains and dosages up to 30 grains had been used. (page 188) The proper dosage is the minimum to relieve symptoms. ___________________ 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. ______________________________ http://www.drlowe.com/frf/t4replacement/intro.htm The most effective of these therapies involves adjusting patients' dosages of combined T4/T3 or T3 alone according to several indices other than TSH and thyroid hormone levels. Those indices are signs, symptoms, and various objective measures of tissue response to particular dosages. When patients' dosages are titrated according to these indices, dosages that prove safe and effective are typically TSH-suppressive.[44] Evidence is available that this therapeutic approach relieves patients' signs, symptoms, and measurable tissue abnormalities such as low resting metabolic rates (RMR) according to indirect calorimetry. This observation suggests that dosages higher than those dictated by the replacement concept more effectively relieve patients' hypothyroid symptoms. Other research has shown that patients report feeling better with TSH-suppressive dosages of thyroid hormone.[23] [24][25] Moreover, psychiatrists report that dosages of T3 higher than replacement dosages augment the depression-relieving effects of antidepressants.[9][28][29][30][31][34] In addition, in a study of patients made hypothyroid by therapeutic destruction of the thyroid gland, some used TSH-suppressive dosages of thyroid hormone and others used T4-replacement. Those on TSH-suppressive dosages didn't gain excess weight; those on T4-replacement did. The researchers concluded that T4-replacement was the cause of the excess weight gain.[55] These published reports are consistent with thousands of cases in which hypothyroid patients recovered from their symptoms and other health problems with TSH-suppressive dosages of thyroid hormone after T4-replacement failed to help them. Kaplan's observation also suggests another point: that T4- replacement keeps many hypothyroid patients' dosages too low to relieve their symptoms is an indictment of the concept of replacement. As the cause of (1) the continued suffering and debility of patients, (2) an increased incidence of potentially life-threatening diseases, and (3) the need for the chronic use of medications, ___________________________ Dr. Derry article: http://thyroid.about.com/library/derry/bl11.htm The effective dose physicians used by clinical judgment and experience before 1975 was around 2-3 times higher than the dose used by TSH blood test monitoring. So everyone's dose of thyroid after 1975 was decreased by about two thirds of well established clinically effective doses. __________________________ Another Derry article: http://thyroid.about.com/library/derry/bl4a.htm In the 1960s it was textbook material after 70 years of experience using thyroid that a dose below 180 mg of desiccated thyroid (3 grains) could not be measured clinically or in the laboratory. In other words it was without effect.(2) The approximate equivalent dose of synthroid or thyroxine (T4) would be about 180 micrograms. (3) So unless your dose is above 180 there is little chance of regaining your hair back and the problem likely continue and get worse. You can tell when you are approaching the right dose personally when the itching starts to go away permanently. Depending on how old you are and other medical history it is likely though you would get complete relief with a dosage up around 200 micrograms of Synthroid or higher. We know that there are no side effects at those dosages. Dosages of thyroxine (Synthroid, T4) of up to 300 micrograms are without morbidity or mortality. (no sickness or deaths) (4) _____________________________ Dr. Lowe's wife: http://www.drlowe.com/emailnewsletter/2003archive.htm Instead, they adjust dosages according to how patients respond to a particular dose. As studies have shown, this approach produces far superior treatment results than does adjusting dosages according to thyroid test results.[1][2] ___________________________ Dr. Lowe uses this guide: http://www.drlowe.com/clincare/clinicalforms/areyouoverstimulated.pdf to determine if the patient is on too high a dose. In other words, they raise thyroid dose up untill the patient feels best and use this form as a way to make sure they haven't gone too high. Dose is determined purely by how the patient feels and no tests are used _____________________ Author: JAMES C. WREN, M.D. Date Published: 01-Jan-1971 Publication: JOURNAL OF THE AMERICAN GERIATRICS SOCIETY Vol. 19, No 1, p 7, 1971 Title: SYMPTOMATIC ATHEROSCLEROSIS: PREVENTION OR MODIFICATION BY TREATMENT WITH DESICCATED THYROID All patients were given desiccated thyroid in an initial dosage of 15 to 30 mg daily (single dose). This was increased slowly to 60 to 240 mg (4 grains) daily (single dose) within six months, the aim being full replacement or physiological dosage. The final dosage was a matter of clinical judgement rather than laboratory study. In most cases the dosage at six months was maintained throughout the rest of the study. In the majority of cases the daily dosage was 120 mg (104 patients) or 180 mg (190 patients). RESULTS Subjective findings General. In the symptomatic group, 100 of 132 patients reported benefit from thyroid therapy, in the form of an increased sense of well-being, increased exercise tolerance, greater motivation and greater alertness. Twenty-two remained unchanged and 10 died. It is generally conceded that human atherosclerosis is irreversible, but these results indicate that the administration of thyroid may be of benefit in many cases. Probably of most importance and significance was the statistical observation that for these thyroid-treated patients the mortality rate was lower than that for the population at large. (Note the doses. They are quite high on average.) _________________________ Report by by Dr. Hertoghe on his studies of thyroid function Daily production of T4 is about 80 to 100 micrograms and T3 is 20 micrograms. (This is equivelent to 3 grains and does not take into account the amount of thyroid that would be lost to the digestive system by taking pills. It is only measuring actual levels in the blood.) _______________________ email correspondence, January 20, 8:33 am 2005 Dear Leitita Wetterauer, according to the ROCHE medical encyclopedia, the daily turnover of T3 and T4 is 30 and 80 microgramm respectively. I don't have further information, but I think you can find plenty of data in the web. Best regards G. Proehl Dr. Gerhard Proehl GSF-Institute of Radiation Protection Postfach 1129 D-85758 Neuherberg Phone: +49-89-3187-2889 Fax: +49-89-3187-3363 Email: proehl@... (This is equivelent to 200 mcg or just under 3 grains. This does not take into account losses to the digestive system by taking pills.) ______________________ Dr. Guberman http://drguberman.com/news.cfm?date_range=8/01/04 7051 West Commercial Blvd., Suite 3-C Tamarac, FL 33319 e-mail: drguberman@... That optimal dosage range is highly individual, but historically, the typical patient's therapeutic window has been somewhere between 120 to 240 mg (2 to 4 grains). There's no way to accurately predict what your therapeutic window is. Until you find it, you may not improve much from the Armour. But once you do, you're likely to feel that the wait was well worth it. _________________________ Author: P. B. S. Fowler Date Published: 11-Aug-1973 Publication: BMJ 11 August 1973 Vol. III p 352 - 353 Title: LETTER: Treatment of Hypothyroidism this infrequent phenomenon lies in the fact that exogenous thyroid hormone in moderate doses administered to normal subjects rarely has appreciable effects, owing to compensatory suppression of the subject's own thyroid gland through diminished secretion by the pituitary of thyroid-stimulating hormone (TSH). TIns feedback inhibition tends to maintain a constant level of circulating thyroid hormone. There are, in fact, instances of normal subjects who have taken quite appreciably excessive doses of thyroid with minimal or no manifestations of toxicity, probably due to enhanced ability for degradation of excessive 84 amounts of hormone in some individual __________________________ http://www.thyroid-info.com/articles/dommisse.htm An Interview with Dommisse, MD Unique Theories About Hypothyroidism Treatment I ran into too many patients who had classic hypothyroid symptoms, which cleared completely on appropriate thyroid treatment, and whose TSH was below 2.0 (but above 1.5) and with FT4 and FT3 levels in the low ends of their 'normal ranges'….Finally, I found some patients with several symptoms and signs of hypothyroidism whose TSH was between 1.0-1.5; so I lowered my range, for the last time, to 0.1- 1.0; I now treat primary hypothyroidism with a TSH of >1.0 (if the FT4 and FT3 are low-normal, not above the middle of their 'normal ranges'). _______________________ .. " Optimum Diagnosis and Treatment of Hypothyroidism With Free T3 and Free T4 Levels " by Dr. ph Mercola (US), DO http://www.mercola.com/article/hypothyroid/diagnosis_comp.htm Most patients continue to have classic hypothyroid symptoms because excessive reliance is placed on the TSH. This test is a highly accurate measure of TSH but not of the height of thyroid hormone levels. The basic problem that traditional medicine has with diagnosing hypothyroidism is the so called " normal range " of TSH is far too high: Many patients with TSH's of greater than 1.5 (not 4.5) have classic symptoms and signs of hypothyroidism. ______________________ Dr. Derry http://thyroid.about.com/library/derry/bl11.htm Topic: Low Adrenal Function and Thyroid Problems Physicians before 1975 found the minimum clinically effective dose for hypothyroid patients was about 180 mg of desiccated thyroid or 180 micrograms of eltroxine (T4). ____________________ Dr. Derry article: http://thyroid.about.com/library/derry/bl4a.htm In the 1960s it was textbook material after 70 years of experience using thyroid that a dose below 180 mg of desiccated thyroid (3 grains) could not be measured clinically or in the laboratory. In other words it was without effect.(2) The approximate equivalent dose of synthroid or thyroxine (T4) would be about 180 micrograms.(3) So unless your dose is above 180 there is little chance of regaining your hair back and the problem likely continue and get worse. We know that there are no side effects at those dosages. Dosages of thyroxine (Synthroid, T4) of up to 300 micrograms are without morbidity or mortality. (no sickness or deaths) (4) _____________________ Dr. Derry http://www.bites-medical.org/hypo/hist.html (Site now gone) There were no problems with desiccated thyroid even at high doses, and it was known as one of the safest drugs available. Synthetic T4, on the other hand, has had a long history of manufacturing and reliability problems. _____________________ (This paper points out that some patients need suppressive doses of thyroid to feel good.) MINI REVIEW Intrinsic imperfections of endocrine replacement therapy J A Romijn, J WA Smit and S W J Lamberts Department of Endocrinology, Leiden University Medical Center, Leiden and Department of Internal Medicine, Erasmus Medical Center, Rotterdam University, Rotterdam, The Netherlands (Correspondence should be addressed to J A Romijn; Email: j.a.romijn@...) However, many patients treated for endocrine insufficiencies still suffer from more or less vague complaints and a decreased quality of life. It is likely that these complaints are, at least in part, caused by intrinsic imperfections of hormone replacement strategies in mimicking normal hormone secretion. ......effects of hormones in general, and thus of hormone replacement strategies in particular, are difficult to quantify at the tissue level. Therefore, in clinical practice we rely mostly on plasma variables – `plasma endocrinology' – which are a poor reflection of hormone action at the tissue level. Complaints of thyroid patients....They range from musculoskeletal complaints, to vague feelings of being unwell, and to depression. Two approaches have been used to decrease the complaints experienced by these patients: an increase in the dose of L-thyroxine, and combination treatment of thyroxine with tri-iodothyronine. In some of the patients, a decrease in complaints can be achieved by increasing the dose of thyroxine above that required to restore TSH concentrations to normal (1). For this reason, such patients are often allowed to take a dose of thyroxine that would be judged as overtreatment with respect to TSH concentrations. The second approach was evaluated by Bunevicius et al. (2), who performed a randomised controlled trial to compare the effects of thyroxine alone with those of thyroxine plus tri-iodothyronine. Patients with hypothyroidism benefitted when 12.5 mg triiodothyronine was substituted for 50 mg thyroxine in their treatment regimens. This resulted in improved neuropsychological functioning. Pulse rates and serum sex hormone-binding globulin concentrations were greater after treatment with thyroxine plus tri-iodothyronine, indicating a slightly greater effect on the heart and liver. Serum thyroxine concentrations were lower and tri-iodothyronine concentrations were greater after treatment with thyroxine plus tri-iodothyronine, but serum TSH concentrations, a sensitive measure of thyroid hormone action, were similar after the two treatments. It should be noted that not all patients benefitted from this approach because, even in the group with combination therapy, patients continued to report complaints of depression. Thyroxine: The thyroid secretes tri-iodothyronine (T3) (,20%) in addition to thyroxine (T4) (,80%). In the absence of thyroid function, exogenous thyroxine is not able to normalise the concentrations of T4 and T3 in all tissues in rodents, even in the presence of normal TSH concentrations. Despite this knowledge, currently available preparations of T3 have unfavourable pharmacological profiles and adequate markers of biological effect are lacking. Additional evidence is required before combination therapy can be advised. First, it is remarkable that the normal values of TSH show a more than tenfold variation, between 0.4 and 4.5mU/l. Because, in clinical practice, the optimal TSH concentration for individual patients within this range is unknown, titration of the substitution dose of thyroxine within this tenfold variation is relatively crude. Secondly, the intrinsic assumption of many doctors in this approach is that normal TSH concentrations reflect adequate thyroid hormone concentrations, not only at the tissue level of the hypothalamus and the pituitary, but also in the other tissues. However, it is likely that this assumption is erroneous, because TSH is produced only by the pituitary gland and therefore may not reflect thyroid hormone status in tissues outside the hypothalamo– pituitary axis. This notion is supported by data obtained from animal experiments. Thyroxine is considered to be an inactive hormone, because a thyroxine-specific receptor has not been identified. Rather, thyroxine serves as a prohormone, because it is the precursor of tri-iodothyronine. Some tissues, such as muscle, have a relatively low deiodinase activity and are dependent, to a great extent, on tri-iodothyronine derived from the thyroid and the liver. In rodents, it has been clearly demonstrated that there is no single dose of thyroxine or tri-iodothyronine that normalises thyroid hormone concentrations in all tissues simultaneously in hypothyroid animals (3). Therefore, it is highly likely that, in patients treated with L-thyroxine, subtle derangements at the tissue level are present with respect to thyroid hormone availability, and probably also thyroid hormone action. _______________________ Changes in serum triiodothyronine, thyroxine, and thyrotropin during treatment with thyroxine in severe primary hypothyroidism M Maeda, N Kuzuya, Y Masuyama, Y Imai and H Ikeda J. Clin. Endocrinol. Metab., Jul 1976; 43: 10 - 17. It is difficult to assess what is the optimal dose for any one subject, for at present we have no objective, easily quantifiable parameter to assess response of body tissues to thyroid hormone replacement. Measurements of serum TSH, kinetics of reflex time, and oxygen consumption are helpful, but not entirely reliable for this purpose. Individuals on physiological replacement replacement doses of pure sodium levothyroxine have elevated levels (high normal to hyperthyroid range) of serum thyroxine (-Pattee). The resin uptake tests in these persons are also elevated above normal, so that in patients on 300 or 400 pg of sodium levothyroxine (4.0 to 5.5 grains) a day, the PBI or serum thyroxine level will be in the high range and so will the free thyroxine index. (Note the very high doses of Synthroid needed to make the patient feel well. This was before over reliance on the TSH test.) _______________________ (This paper points out that healthy people have little responxe to being given thyroid.) Author: WILLIAM H. BEIERWALTES, M.D. Date Published: 01-Jan-1955 Publication: Michigan Journal Clinical Endocrinology Vol. 15, 1955 p148 - 150 (Editorial) Title: RESPONSE TO THYROID Category: diagnosing Keywords: thyroid, BEIERWALTES, desiccated, oral, research, myxedqamatous, myxoedema, euthyroid , diagnose, basal, pulse rate, iodine Text: 1955 Editorial WILLIAM H. BEIERWALTES, M.D. University Hospital, Ann Arbor, Michigan Journal Clinical Endocrinology Vol. 15, 1955 p148 - 150 p148 RESPONSE TO THYROID WHEN desiccated thyroid is administered orally to myxedematous humans, the resultant metabolic changes are quite different from those observed in the euthyroid subject. The clinician can diagnose or treat hypothyroid patients much more intelligently if he is aware of these difference in response to thyroid. In addition, an unworked field for clinical research becomes evident when one reviews the known major differences between the myxedematous patient and the euthyroid subject in response to desiccated thyroid administration. The most striking difference observed may be summarized by the statement that the patient who is truly deficient in circulating thyroid hormone responds dramatically and with predictable regularity to the administration of small doses of desiccated thyroid. The euthyroid subject, on the other hand, shows no obvious clinical response to small doses of thyroid. A simple and readily available diagnostic test for borderline hypothyroidism, therefore, is the administration of 1 grain of desiccated thyroid per day for a period of six weeks after a careful history and physical examination have been made and basal metabolic rate and serum cholesterol determinations have been performed. The patient who is truly deficient in thyroid hormone will generally respond to the administration of 1 grain of desiccated thyroid per day for six weeks with an increase in basal pulse rate and metabolic rate and a fall in the serum cholesterol level. The patient not truly deficient in thyroid hormone will show no significant change in these indices of thyroid hormone effect. p149 .....The myxedematous patient and the euthyroid subject also show a different response to sudden cessation of desiccated thyroid medication. The myxedematous patient at first shows a rapid drop in his serum precipitable-iodine level and basal metabolic rate, then a slower fall to pre-treatment levels over a period of six to eight weeks (3). On the other hand, when the thyroid medication of a euthyroid person is suddenly stopped, the serum precipitable-iodine value falls to myxedematous levels in three to four weeks, but the basal metabolic rate may take as long as nine to fifteen weeks to reach its lowest level (3). These values then rise to pre-treatment levels. The radioiodine uptake is also falsely depressed by thyroid administration and has taken as long as eleven weeks to recover (4). Furthermore, when the thyroid does recover its ability to concentrate I131, the I131 pickup rate may rebound temporarily to hyperthyroid levels. Obviously, if a physician were to stop the desiccated thyroid medication of a euthyroid patient in an attempt to evaluate the patient's underlying thyroid status, these ensuing changes in indices of thyroid function, when sampled, might prove very misleading and confusing. The daily output of thyroid hormone by the normal thyroid gland is thought to be equivalent to not more than 3 grains of desiccated thyroid per day. Consequently, when the daily dosage of desiccated thyroid is raised to 4 grains or more per day, any differences observed between athyreotic and euthyroid subjects can not be explained on the basis of further suppression of normal thyroid function. Most practicing physicians have probably observed a euthyroid patient who was comfortable while voluntarily taking 5 to 20 grains of desiccated thyroid a day, in an attempt to reduce p149 his weight and rid himself of fatigue. Rarely, if ever, does one see an athyreotic patient voluntarily take more than 3 grains of desiccated thyroid per day. This situation suggests that the athyreotic patient is more sensitive to thyroid substance than is the euthyroid person, even after his myxedema has been controlled with medication. .....WILLIAM H. BEIERWALTES, M.D. University Hospital, Ann Arbor, Michigan REFERENCES 1. MEANS, J. H,: The Thyroid and Its Disease, ed. 2. Philadelphia, J. B. Lippincott Co., 1948, p 249 2. WINKLER, A. W.; RIGGS, D. S., and MAN, E. B.: Serum iodine in hypothyroidism before and during thyroid therapy, J. Clin. Invest. 24: 732, 1945 3. RIGGS, D. S.; MAN, E. B., and WINKLER, A. W.: Serum iodine of euthyroid subjects treated with desiccated thyroid, J. Clin. Invest. 24: 722, 1945 4. GREER, M. A.: The effect on endogenous thyroid activity of feeding desiccated thyroid to normal human subjects, New England J. Med. 244: 385, 1951 5. JOHNSTON, M. W.; SQUIRES, A. H., and FARQHARSON, R. F.: The effect of prolonged administration of thyroid, Ann. Int. Med. 35: 1008, 1951 6. THOMPSON, W. O.; THOMPSON, P. K.; TAYLOR, S. G., and DICKIE, L. F. N.: Calorigenic action of single large doses of desiccated hog thyroid: comparison with the action of thyroxine given orally and intravenously, Arch. Int. Med. 54: 888, 1934 Quote Link to comment Share on other sites More sharing options...
Guest guest Posted March 2, 2005 Report Share Posted March 2, 2005 In a message dated 3/2/2005 3:14:51 PM Eastern Standard Time, saltillo@... writes: > Nobody has ever looked at whether the > patient did better long-term on the new lower doses compared to the > older higher doses. It's amazing to me that they could make this > change without anything to back it up or to make sure the change was > wise. yep. yep. yep. but what is really bad is that the PDR has only up to 3 grains for severe hypo. and that information has to come from the manufacturer i would think - and where the heck did they get that info? cindi Quote Link to comment Share on other sites More sharing options...
Guest guest Posted March 2, 2005 Report Share Posted March 2, 2005 In a message dated 3/2/2005 3:14:51 PM Eastern Standard Time, saltillo@... writes: > Nobody has ever looked at whether the > patient did better long-term on the new lower doses compared to the > older higher doses. It's amazing to me that they could make this > change without anything to back it up or to make sure the change was > wise. yep. yep. yep. but what is really bad is that the PDR has only up to 3 grains for severe hypo. and that information has to come from the manufacturer i would think - and where the heck did they get that info? cindi Quote Link to comment Share on other sites More sharing options...
Guest guest Posted March 2, 2005 Report Share Posted March 2, 2005 In a message dated 3/2/2005 3:14:51 PM Eastern Standard Time, saltillo@... writes: > Nobody has ever looked at whether the > patient did better long-term on the new lower doses compared to the > older higher doses. It's amazing to me that they could make this > change without anything to back it up or to make sure the change was > wise. yep. yep. yep. but what is really bad is that the PDR has only up to 3 grains for severe hypo. and that information has to come from the manufacturer i would think - and where the heck did they get that info? cindi Quote Link to comment Share on other sites More sharing options...
Guest guest Posted March 2, 2005 Report Share Posted March 2, 2005 > thanks for posting all this great info...i'd printed out some of this before > when you posted some items - but great to see it all together...all 18 pages! ______________- I started collecting this when I developed bursitis on 2 grains and was not getting better. Then I read two articles about this being a sign of low thyroid and that in the past doses were much higher. I could not tolerate thyroid well in the beginning and could only make 1/8th grain raises. But, after realizing that low dose therapy was not effective for many, I slowly worked on getting my dose up. When I got to 3 grains, my whole life just became so much better and I began to finally feel normal. My adrenal issues really improved. So, I have been trying to collect dose and thyroid production info for a while now. Tish Quote Link to comment Share on other sites More sharing options...
Guest guest Posted March 2, 2005 Report Share Posted March 2, 2005 > thanks for posting all this great info...i'd printed out some of this before > when you posted some items - but great to see it all together...all 18 pages! ______________- I started collecting this when I developed bursitis on 2 grains and was not getting better. Then I read two articles about this being a sign of low thyroid and that in the past doses were much higher. I could not tolerate thyroid well in the beginning and could only make 1/8th grain raises. But, after realizing that low dose therapy was not effective for many, I slowly worked on getting my dose up. When I got to 3 grains, my whole life just became so much better and I began to finally feel normal. My adrenal issues really improved. So, I have been trying to collect dose and thyroid production info for a while now. Tish Quote Link to comment Share on other sites More sharing options...
Guest guest Posted March 2, 2005 Report Share Posted March 2, 2005 > thanks for posting all this great info...i'd printed out some of this before > when you posted some items - but great to see it all together...all 18 pages! ______________- I started collecting this when I developed bursitis on 2 grains and was not getting better. Then I read two articles about this being a sign of low thyroid and that in the past doses were much higher. I could not tolerate thyroid well in the beginning and could only make 1/8th grain raises. But, after realizing that low dose therapy was not effective for many, I slowly worked on getting my dose up. When I got to 3 grains, my whole life just became so much better and I began to finally feel normal. My adrenal issues really improved. So, I have been trying to collect dose and thyroid production info for a while now. Tish Quote Link to comment Share on other sites More sharing options...
Guest guest Posted March 2, 2005 Report Share Posted March 2, 2005 >(now at >54 1/2 grains and some Cytomel) >And then the doctor wanted to >reduce that. Uhhh...54 1/2 grains? I think I can see why he wanted to cut you back! Laurie Quote Link to comment Share on other sites More sharing options...
Guest guest Posted March 2, 2005 Report Share Posted March 2, 2005 I don't think these old sources are wrong. __________________ I agree. Back then they adjusted medication by how the patient felt and how heatlhy they appeared along with other physical measures. This worked quite well for considerably more years than the new lower dose methods of today. Nobody has ever looked at whether the patient did better long-term on the new lower doses compared to the older higher doses. It's amazing to me that they could make this change without anything to back it up or to make sure the change was wise. Just trusting that the TSH test was more accurate is hardly good enough. Tish Quote Link to comment Share on other sites More sharing options...
Guest guest Posted March 2, 2005 Report Share Posted March 2, 2005 I don't think these old sources are wrong. __________________ I agree. Back then they adjusted medication by how the patient felt and how heatlhy they appeared along with other physical measures. This worked quite well for considerably more years than the new lower dose methods of today. Nobody has ever looked at whether the patient did better long-term on the new lower doses compared to the older higher doses. It's amazing to me that they could make this change without anything to back it up or to make sure the change was wise. Just trusting that the TSH test was more accurate is hardly good enough. Tish Quote Link to comment Share on other sites More sharing options...
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