Guest guest Posted February 25, 2005 Report Share Posted February 25, 2005 Don't sit in the corner! I just didn't respond as I am NOT real knowledgeable in adrenal issues... TISH???? Artistic Grooming Hurricane, West Virginia Quote Link to comment Share on other sites More sharing options...
Guest guest Posted February 25, 2005 Report Share Posted February 25, 2005 did you have any coffee, tea, soda pop, toothpaste on a tooth brush, chocolate or OJ prior to the morning saliva test? Are you on any adrenal supplements or steroidss? Lab Results/2nd Post Hi, I posted these earlier but didn't get any replies. :0( After I post them I'll go and sit in the corner. 7:00-8:00 AM 27 Elevated (13-24nM) 11:00-12:00 PM 3 Depressed (5-10nM) 4:00-5:00 PM 7 Normal (3-8nM) 11:00-11:59 PM 1 Normal (1-4nM) My DHEA was 2 Depressed (Adults (M/F) 3-10 My dr said to take 7-keto (25 mgs) and to take melatonin to help me to fall asleep. I tried the melatonin but I'm still wide awake at midnight. Which means I'm tired in the morning. I'd appreciate any help on this matter. (I hate drs) Thanks, Sue in dreary Austin, Tx. Quote Link to comment Share on other sites More sharing options...
Guest guest Posted February 25, 2005 Report Share Posted February 25, 2005 did you have any coffee, tea, soda pop, toothpaste on a tooth brush, chocolate or OJ prior to the morning saliva test? Are you on any adrenal supplements or steroidss? Lab Results/2nd Post Hi, I posted these earlier but didn't get any replies. :0( After I post them I'll go and sit in the corner. 7:00-8:00 AM 27 Elevated (13-24nM) 11:00-12:00 PM 3 Depressed (5-10nM) 4:00-5:00 PM 7 Normal (3-8nM) 11:00-11:59 PM 1 Normal (1-4nM) My DHEA was 2 Depressed (Adults (M/F) 3-10 My dr said to take 7-keto (25 mgs) and to take melatonin to help me to fall asleep. I tried the melatonin but I'm still wide awake at midnight. Which means I'm tired in the morning. I'd appreciate any help on this matter. (I hate drs) Thanks, Sue in dreary Austin, Tx. Quote Link to comment Share on other sites More sharing options...
Guest guest Posted February 25, 2005 Report Share Posted February 25, 2005 Maybe I can help you. You have adrenal fatigue and it is causing you to loose your circadian rythem. When this happened to me nothing seemed to work to help me sleep. Melatonin just made me sleepy but unable to sleep. Your doctor's advice was goo however. When you loose your circadian rythem from adrenal fatigue, you don't make melatonin. > 7:00-8:00 AM 27 Elevated (13-24nM) > > 11:00-12:00 PM 3 Depressed (5-10nM) > > 4:00-5:00 PM 7 Normal (3-8nM) > > 11:00-11:59 PM 1 Normal (1-4nM) > > My DHEA was 2 Depressed (Adults (M/F) 3-10 _____________________________ What happens when the adenals have more demand on them than they can do is that they go into a kind of drastic up and down production, with periods of high production followed by low production. Then, later in the day, the body needs a lot less cortisol, so the adrenals can often handle it then. The healthy human adrenal gland makes about double the cortisol in the morning of the rest of the day. So, demand is very high in the morning and by evening it is quite low. By 12:00 3:00 in the morning cortisol levels are at the lowest point of the day. This is the common period when adrenal fatigue people will wake and not be able to get back to sleep. But, when adrenal fatigue is bad enough, you can't sleep at all. I became a total insomniac when I started thyroid. After a month of no sleep, I begged my husband to take me to the hospital to have me put to sleep. It can get really bad. Add on top of this that not sleeping can double the demands for cortisol and actually make everything so much worse. The low DHEA goes along with adrenal fatigue. Typically it is either too low or too high. The reason the adrenals are so irratic in adrenal fatigue has to do with demand for cortisol and other adrenal hormones being higher than the gland can make. So, at some point in the day or with some stress, the gland becomes depleted of it's hormones and has to stop production to rebuild them. When they do this, the brain senses that there is not enough cortisol in the blood and it starts to put out ACTH to try to stimulate the adrenals to put out hormone. But, they can't untill they are ready. So, ACTH builds up in the blood and finally when the adrenals have recovered and made some hormone, they see that there is a lot of ACTH in the blood. They think there is a crisis and so they dump everything they just made and are once again depleted. So, in adrenal fatige, you will get periods of excess production followed by too low of levels. This up and down behavior destroys your natural circadian rythem that prepares the body for sleep. The adrenals need to have a nice smoothe cycle of production where it is high in the morning and then tapers off ever so slowly throughout the day to it's lowest point at about 2:00 in the morning. And then it needs to start all over. This is needed for the body to make melatonin and for the body to properly prepare for sleep and to cool down before bedtime, etc. So, what can you do about it? My first doctor gave me muscle relaxants and sleep pill samples to use untill my adrenals could recover over time. It takes the adrenals a long to recover from this problem. But, I quickly got addicted to these little pink pills and they quit helping me sleep and I wouldn't sleep at all if I didn't take them. This was a real drag. The other thing you can do is adrenal support. Adrenal support is ome type of low dose cortisone therapy. It can be 10 to 20 mg of prescription Cortef a day taken in 4 equal doses every 4 hours or 4 to 8 IsoCort tablets a day taken in 4 equal doses every 4 hours. This is equal to 10 to 20 mg of cortef. You can get this from VitaminMD.com. You can also take 1 teaspoon of licorice root in a tea 4 times a day every 4 hours. This can help give the adrenals enough support to stop this up and down cycling that is ruining your sleep. The down side is that after 4 weeks of this, you are dependent on it and you must then taper off it very slowly over several weeks. It takes about two weeks before you will notice improvements. Adrenal support can last for 4 months to 2 years. But, my experience is that after two years it's hell to get off of. Finally, here are some daily things you can do to take a load off of your adrenals. -avoid sugar, simple carbohydrates and caffeine. These are adrenal killers. -eat small healthy snacks every two hours in the day. -put a healthy snack by your bedside and take a bit every time you need one. Often in adrenal fatigue the person will have hypoglycemia at night. This will not allow the body to sleep. -There are many herbs out there that can help with sleep. however, I have found that they quit working soon. But, they can get you a few nights of good sleep. Try, licorice root, motherwort, skullcap, wild lettuce, hopps, and others. You can find good herbal sleep aids in health food stores. -take a hot bath before bedtime. -reduce stress as much as possible. -lie down for 10 minutes in the day as often as you can. This really helps the adrenals. -I found that the antihistamine Doxylamine succinate works very well, but it lowers thyroid function slightly. -excercise only in short 10 minute sessions and wait an hour or two between. -eat more protein as this is lost in adrenal fatigue. There are more tips that maybe others can supply. Good luck. Tish Quote Link to comment Share on other sites More sharing options...
Guest guest Posted February 25, 2005 Report Share Posted February 25, 2005 Maybe I can help you. You have adrenal fatigue and it is causing you to loose your circadian rythem. When this happened to me nothing seemed to work to help me sleep. Melatonin just made me sleepy but unable to sleep. Your doctor's advice was goo however. When you loose your circadian rythem from adrenal fatigue, you don't make melatonin. > 7:00-8:00 AM 27 Elevated (13-24nM) > > 11:00-12:00 PM 3 Depressed (5-10nM) > > 4:00-5:00 PM 7 Normal (3-8nM) > > 11:00-11:59 PM 1 Normal (1-4nM) > > My DHEA was 2 Depressed (Adults (M/F) 3-10 _____________________________ What happens when the adenals have more demand on them than they can do is that they go into a kind of drastic up and down production, with periods of high production followed by low production. Then, later in the day, the body needs a lot less cortisol, so the adrenals can often handle it then. The healthy human adrenal gland makes about double the cortisol in the morning of the rest of the day. So, demand is very high in the morning and by evening it is quite low. By 12:00 3:00 in the morning cortisol levels are at the lowest point of the day. This is the common period when adrenal fatigue people will wake and not be able to get back to sleep. But, when adrenal fatigue is bad enough, you can't sleep at all. I became a total insomniac when I started thyroid. After a month of no sleep, I begged my husband to take me to the hospital to have me put to sleep. It can get really bad. Add on top of this that not sleeping can double the demands for cortisol and actually make everything so much worse. The low DHEA goes along with adrenal fatigue. Typically it is either too low or too high. The reason the adrenals are so irratic in adrenal fatigue has to do with demand for cortisol and other adrenal hormones being higher than the gland can make. So, at some point in the day or with some stress, the gland becomes depleted of it's hormones and has to stop production to rebuild them. When they do this, the brain senses that there is not enough cortisol in the blood and it starts to put out ACTH to try to stimulate the adrenals to put out hormone. But, they can't untill they are ready. So, ACTH builds up in the blood and finally when the adrenals have recovered and made some hormone, they see that there is a lot of ACTH in the blood. They think there is a crisis and so they dump everything they just made and are once again depleted. So, in adrenal fatige, you will get periods of excess production followed by too low of levels. This up and down behavior destroys your natural circadian rythem that prepares the body for sleep. The adrenals need to have a nice smoothe cycle of production where it is high in the morning and then tapers off ever so slowly throughout the day to it's lowest point at about 2:00 in the morning. And then it needs to start all over. This is needed for the body to make melatonin and for the body to properly prepare for sleep and to cool down before bedtime, etc. So, what can you do about it? My first doctor gave me muscle relaxants and sleep pill samples to use untill my adrenals could recover over time. It takes the adrenals a long to recover from this problem. But, I quickly got addicted to these little pink pills and they quit helping me sleep and I wouldn't sleep at all if I didn't take them. This was a real drag. The other thing you can do is adrenal support. Adrenal support is ome type of low dose cortisone therapy. It can be 10 to 20 mg of prescription Cortef a day taken in 4 equal doses every 4 hours or 4 to 8 IsoCort tablets a day taken in 4 equal doses every 4 hours. This is equal to 10 to 20 mg of cortef. You can get this from VitaminMD.com. You can also take 1 teaspoon of licorice root in a tea 4 times a day every 4 hours. This can help give the adrenals enough support to stop this up and down cycling that is ruining your sleep. The down side is that after 4 weeks of this, you are dependent on it and you must then taper off it very slowly over several weeks. It takes about two weeks before you will notice improvements. Adrenal support can last for 4 months to 2 years. But, my experience is that after two years it's hell to get off of. Finally, here are some daily things you can do to take a load off of your adrenals. -avoid sugar, simple carbohydrates and caffeine. These are adrenal killers. -eat small healthy snacks every two hours in the day. -put a healthy snack by your bedside and take a bit every time you need one. Often in adrenal fatigue the person will have hypoglycemia at night. This will not allow the body to sleep. -There are many herbs out there that can help with sleep. however, I have found that they quit working soon. But, they can get you a few nights of good sleep. Try, licorice root, motherwort, skullcap, wild lettuce, hopps, and others. You can find good herbal sleep aids in health food stores. -take a hot bath before bedtime. -reduce stress as much as possible. -lie down for 10 minutes in the day as often as you can. This really helps the adrenals. -I found that the antihistamine Doxylamine succinate works very well, but it lowers thyroid function slightly. -excercise only in short 10 minute sessions and wait an hour or two between. -eat more protein as this is lost in adrenal fatigue. There are more tips that maybe others can supply. Good luck. Tish Quote Link to comment Share on other sites More sharing options...
Guest guest Posted February 25, 2005 Report Share Posted February 25, 2005 Maybe I can help you. You have adrenal fatigue and it is causing you to loose your circadian rythem. When this happened to me nothing seemed to work to help me sleep. Melatonin just made me sleepy but unable to sleep. Your doctor's advice was goo however. When you loose your circadian rythem from adrenal fatigue, you don't make melatonin. > 7:00-8:00 AM 27 Elevated (13-24nM) > > 11:00-12:00 PM 3 Depressed (5-10nM) > > 4:00-5:00 PM 7 Normal (3-8nM) > > 11:00-11:59 PM 1 Normal (1-4nM) > > My DHEA was 2 Depressed (Adults (M/F) 3-10 _____________________________ What happens when the adenals have more demand on them than they can do is that they go into a kind of drastic up and down production, with periods of high production followed by low production. Then, later in the day, the body needs a lot less cortisol, so the adrenals can often handle it then. The healthy human adrenal gland makes about double the cortisol in the morning of the rest of the day. So, demand is very high in the morning and by evening it is quite low. By 12:00 3:00 in the morning cortisol levels are at the lowest point of the day. This is the common period when adrenal fatigue people will wake and not be able to get back to sleep. But, when adrenal fatigue is bad enough, you can't sleep at all. I became a total insomniac when I started thyroid. After a month of no sleep, I begged my husband to take me to the hospital to have me put to sleep. It can get really bad. Add on top of this that not sleeping can double the demands for cortisol and actually make everything so much worse. The low DHEA goes along with adrenal fatigue. Typically it is either too low or too high. The reason the adrenals are so irratic in adrenal fatigue has to do with demand for cortisol and other adrenal hormones being higher than the gland can make. So, at some point in the day or with some stress, the gland becomes depleted of it's hormones and has to stop production to rebuild them. When they do this, the brain senses that there is not enough cortisol in the blood and it starts to put out ACTH to try to stimulate the adrenals to put out hormone. But, they can't untill they are ready. So, ACTH builds up in the blood and finally when the adrenals have recovered and made some hormone, they see that there is a lot of ACTH in the blood. They think there is a crisis and so they dump everything they just made and are once again depleted. So, in adrenal fatige, you will get periods of excess production followed by too low of levels. This up and down behavior destroys your natural circadian rythem that prepares the body for sleep. The adrenals need to have a nice smoothe cycle of production where it is high in the morning and then tapers off ever so slowly throughout the day to it's lowest point at about 2:00 in the morning. And then it needs to start all over. This is needed for the body to make melatonin and for the body to properly prepare for sleep and to cool down before bedtime, etc. So, what can you do about it? My first doctor gave me muscle relaxants and sleep pill samples to use untill my adrenals could recover over time. It takes the adrenals a long to recover from this problem. But, I quickly got addicted to these little pink pills and they quit helping me sleep and I wouldn't sleep at all if I didn't take them. This was a real drag. The other thing you can do is adrenal support. Adrenal support is ome type of low dose cortisone therapy. It can be 10 to 20 mg of prescription Cortef a day taken in 4 equal doses every 4 hours or 4 to 8 IsoCort tablets a day taken in 4 equal doses every 4 hours. This is equal to 10 to 20 mg of cortef. You can get this from VitaminMD.com. You can also take 1 teaspoon of licorice root in a tea 4 times a day every 4 hours. This can help give the adrenals enough support to stop this up and down cycling that is ruining your sleep. The down side is that after 4 weeks of this, you are dependent on it and you must then taper off it very slowly over several weeks. It takes about two weeks before you will notice improvements. Adrenal support can last for 4 months to 2 years. But, my experience is that after two years it's hell to get off of. Finally, here are some daily things you can do to take a load off of your adrenals. -avoid sugar, simple carbohydrates and caffeine. These are adrenal killers. -eat small healthy snacks every two hours in the day. -put a healthy snack by your bedside and take a bit every time you need one. Often in adrenal fatigue the person will have hypoglycemia at night. This will not allow the body to sleep. -There are many herbs out there that can help with sleep. however, I have found that they quit working soon. But, they can get you a few nights of good sleep. Try, licorice root, motherwort, skullcap, wild lettuce, hopps, and others. You can find good herbal sleep aids in health food stores. -take a hot bath before bedtime. -reduce stress as much as possible. -lie down for 10 minutes in the day as often as you can. This really helps the adrenals. -I found that the antihistamine Doxylamine succinate works very well, but it lowers thyroid function slightly. -excercise only in short 10 minute sessions and wait an hour or two between. -eat more protein as this is lost in adrenal fatigue. There are more tips that maybe others can supply. Good luck. Tish Quote Link to comment Share on other sites More sharing options...
Guest guest Posted February 25, 2005 Report Share Posted February 25, 2005 High T3 and T4 numbers and low TSH on thyroid doses that are less than the gland makes are not true hyperthryodism, but a result of adrenal fatigue or anemia or a deficiency that is interfering with the body's ability to use thryoid. The healthy human thyroid makes 3 to 5 grains a day. When you take less than this or for example 2 grains, the pituitary adjusts TSH to tell the thyroid to make 2 grains less or less than that. So, if you take 2 grains, TSH drops to tell your thyroid to make another 1 to 3 grains or less to get the daily total up to 3 to 5 grains grains or less. So, any time you have trouble with thyroid doses less than 3 grains it is caused by adrenal insufficiency, anemia and/or other deficiencies. This causes thyroid hormone to build up in the blood stream and not be able to get into tissues. So, tissues are starved for thyroid and the blood is awash with it. The results are that tests come back erroniously high and have no correlation at all to your true thyroid status and whether all tissues have enough hormone. Studies done with healthy people with good adrenal function foudn that they were not able to make any changes to thyroid status with thyroid doses less than 3 to 5 grains. This was because the pituitary worked against them by lowering TSH to drop thyroid production by the amount of thyroid taken. So, any time you have trouble with low doses of thyroid, less than 3 grains, it's not true hypothyroidism but a build-up of unusable hormone in the blood. Tests don't measure what's in tissues and organs. The average dose at which most patients feel the best is usually between 3 and 5 grains, with a few people being able to get by on 2 grains. http://thyroid.about.com/library/derry/bl4a.htm Low dose therapy has not been found to be effective at raising the metabolic rate in studies. People who have been hypo a long time are often extreemly sensitive to low doses of hormone. They usually have low adrenal function that is responsible for much of this. Healthy people can take very large doses of thyroid, up to 9 grains with no symptoms of hyperthryoidism. This is because they have good adrenal function and can burn up excess thyroid. Tish ___________________ From " Thyroid Guardian of Health " by G. Young It is an important guidline in that if individuals are placed on and excessive dose of thyroid hormone, the temperature should become elevated within two weeks time. However, if the thyroid feedback mechanisms are working properly it is impossible to make and individual hyperthyroid untill they are given more thyroid that the gland produces--about 4-1/2 grains for a small individual and about 5 grains for the usual adult. Their basal temperature should rise up over 98.2 deg F if they are truely hyperthyroid, and thus have too much thyroid hormone. The pulse is important as well; a slow pulse is typical of pure low thyroid condition. With low adrenal function, the pulse speeds up and the rapid pulse may indicate inadequate adrenal support. The blood pressure is also an important guid line. A blood pressure with a systolic below one hundred indicates inadequate adrenal support...... Some authorities believe that if autoantibodies are present, it renders other thyroid testing invalid. Clinical symptoms remain the best indicator of adequate dosage. __________________________________ Barry Durrant Peatfield " The Great Thyroid Scandal " Page 101 We saw earlier that the thyroid hormones have to be processed in the body to work; the chief one, thyroxine (T4) has to be converted into the active thyroid hormone triiodothyronine (T3), under the action of the two 5'-diodinase enzymes. With a low adrenal reserve this reaction doesn't proceed as it should, and the body may become toxic with unused and unusable T4. The problem doesn't end there: the T3 has to be taken up by the receptors within the cell wall, to be passed into the cell. This uptake is degraded in adrenal insufficiency; the receptors become dormant or may disappear or may become resistant. In this situation, even if T3 is available, the system can become toxic if it cannot be used properly. You can see how desperately important the adrenals are; and equally how important it is to provide adrenal support, in the form of cortisone supplementation when low adrenal reserve is present. I must tell you now that the failure of thyroid supplementation to restore normal health may well be largely down to the adrenal problem. ___________________ 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 ___________________________ (This article show 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. Quote Link to comment Share on other sites More sharing options...
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