increasing core temperature [Forum Archive]

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increasing core temperature

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Posted by: hardasnails1973

I have been suffering with this problem for almost5 months and dr's are not helping. All my test have come back in the range for thyroid but my body temperature is 96.5 degrees average in the morning, losing hair, depressed, muscle aches , cold feet and hands, constipation, slow digestion you name it i got it.

This is my course of action

1. iodine test for lack of iodine (needed to convert t-4 to t-3)
2. add 12.5 mcgs of t-3 and monitor core temperature till it gets to 98.6 in the morning (this will allow chemical actions to take place more efficently ) and allow me to clear my liver colon of any toxins
3. do a liver flush when bowels are moving and to flush any stones out of my liver/gallbladder (this is where conversions of t4-t3 take place)

4 diet is 45 p/30f /25c body has lost 20 lbs of lean muscle mass in 5 months low test levels but once i get thyroid under control and increased i have an idea from chemical reactions it will come back up. All the test results are indicating this, but there seem to be a missing variable some where and drs can not find it, adrenals check out okfrom cortisol,and dhea test.

yes i used gh w/o t-3, with ECA stack with low caloires under alot of emotional and physical stress and i know this was contributing factor

Posted by: Dale Mabry

Which Thyroid test did you have done?

How much of a contributing factor would you say the GH was?

Posted by: hardasnails1973

i found out gh and EC stack, low caloires, stress slow down t4- t3 conversion so I would say it was a major one to tell truth ..

Posted by: Dale Mabry

Did you check out Cushing's Syndrome, I think I posted something about it on here somewhere. That has to do with the conversion of T4 to T3.

Posted by: Mudge

Sounds like one way to avoid this problem is using 5 on 2 off protocol.

Posted by: hardasnails1973

i just got results back testosterone 91 total igf levels perfect, i used that protocol for gh you mean for the ephederine,caffine stack ?

Posted by: Mudge

Oh nope, I meant for GH. There is a posting on ology about how to try and avoid becoming a diabetic etc from GH.

BiggieSwolls would have posted it I believe.

Posted by: chiquita6683

*gawd DAMN! u guys r geniouses!!!!!!!!!!!!!!!!!!

yea

member like im only 20!

Posted by: chiquita6683

Dale Mabry

*just spreadin mah luuuuuvvv

Posted by: chiquita6683

EEEEEEEEEHHHH! whatup Mudgy? BABY!!!!!!!
LIKE=like*
Did You no that ura Stud?!

Posted by: chiquita6683

HANs!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!! !!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!! o,ummmm*Wait* !!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!! !! !!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!! !!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!! !!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!*sig h*!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!

omg I am just like 2 DAMN Cute!!!!!!!!!!!!!!!!!!

*ok retards! i was showin some Love 4 Hardasnails1973
w the xclamations!!!!!!!!!!!!!!!
*flutters eyelashes*

Posted by: hardasnails1973

don't need love need answers..at end of my rope .. have to o for MRI to rule of tumor (waste of time). i suggested some GnHR analog and he kinda gave me a funny look.

Posted by: chiquita6683

Quote:

Originally posted by hardasnails1973
I have been suffering with this problem for almost5 months and dr's are not helping. All my test have come back in the range for thyroid but my body temperature is 96.5 degrees average in the morning, losing hair, depressed, muscle aches , cold feet and hands, constipation, slow digestion you name it i got it.

This is my course of action

1. iodine test for lack of iodine (needed to convert t-4 to t-3)
2. add 12.5 mcgs of t-3 and monitor core temperature till it gets to 98.6 in the morning (this will allow chemical actions to take place more efficently ) and allow me to clear my liver colon of any toxins
3. do a liver flush when bowels are moving and to flush any stones out of my liver/gallbladder (this is where conversions of t4-t3 take place)

4 diet is 45 p/30f /25c body has lost 20 lbs of lean muscle mass in 5 months low test levels but once i get thyroid under control and increased i have an idea from chemical reactions it will come back up. All the test results are indicating this, but there seem to be a missing variable some where and drs can not find it, adrenals check out okfrom cortisol,and dhea test.

yes i used gh w/o t-3, with ECA stack with low caloires under alot of emotional and physical stress and i know this was contributing factor

ummm..............like i cant underdstand Any of That/this Shit.
and but i will say THIS*

[Q]This is my course of action[/Q]

LIKE its ok that i cant Understand it Now...........ALL I GOT IS TIME BABY!!!!! yea u know who you r, U STUD[b]S[b]!!!!!

k yea im very sorry/i do apologize if this Thread Just ENDS ABRUPTLY! han, was just on my buddy list, bc hes my friend!!!!!

And i mean Han, cmon BABY!
u know You love Mee!!!!!! and ummmm................
oh! u were the 1 that introduced me to iron mag

Posted by: chiquita6683

eeeeeeeeeehhhh!!!!!!!!!
Like omg ur Sooooooooo Smart!
*and Mature*

Posted by: Mudge

Quote:

Originally posted by hardasnails1973
GnHR analog and he kinda gave me a funny look.

I'm sure your doc is not used to patients diagnosing themselves, thats a good one.

I think your idea is a good one, you may even need more T3 though dunno. HRT is 25-50mcg or so depending on bodyweight, male or female etc, a woman at work is on synthroid but I forget the breakdown.

Posted by: hardasnails1973

was thinkig 1/2 a grain of armour. but nandi12 also suggested the Gnrh as well, but how is it administred if you have to have pulse every 2 hours or is it just done at dr's office. if pituirry is alseep it would make sense my body is running at half speed.

Posted by: chiquita6683

Quote:

Originally posted by hardasnails1973
don't need love need answers..at end of my rope .. have to o for MRI to rule of tumor (waste of time). i suggested some GnHR analog and he kinda gave me a funny look.

Like Omg!*

*sigh* I really DO no WHAT ITs LIKE when Your Sick!

*[

hey IM EDITING

BUT HAN PROBLY KNOWS THAT!!!!!!!

Posted by: Mudge

Nandi is definitely one to lend an ear to, you're in good hands.

Posted by: hardasnails1973

Lifestyle: T4 is made by the thyroid and secreted into the bloodstream. The T4 travels to the cells to be converted to T3. Instead of converting all the T4 to T3 it converts some of it to reverseT3 (rT3), which is an inactive form. It usually does this as a response to stress (metabolic or any other kind) and responds as if the body were in famine. T3 causes you to burn off more sugar and fat as e
and fat as energy, but rT3 will not, thus conserving energy. This is most commonly seen in undernourished/malnourished people. If treated with thyoid medication, this will actually create more hormone imbalances because you are already making enough T3 already and do not need to replace a hormone you are already making. Upon taking thyroid med for this, one would initially feel better, but after a while would begin feeling bad again. Correcting nutritional status should remedy this form of hypothyroidism.

I belive this is what has happened to me on top of crashing. Shut my self down frm uder eating and stress and now metabolic activites are not taking place so reactions can work..

I did Iodine test and patch was gone in 8 hours !! so this makes me lead to my body is defiicent in sme thing and or is not absorbing it becuase of slow metabolism from lazy pituitary, mudge do you know about anythng about GnRH therapy. It keeps saying about some thing like pulses every 2 hours with an infusion pump?

Posted by: hardasnails1973

Nutrition
Since thyroid hormone plays a central role in the regulation of total body metabolism, it is not surprising that various nutritional factors may profoundly alter the regulation, supply, and disposal of this thermogenic hormone. Although many dietary changes can affect the thyroid economy, the most striking and important effects are related to alterations in total caloric intake and the supply of iodine. The changes associated with caloric deprivation appear homeostatic in nature, producing alterations in thyroid hormones which would conserve energy through a reduction in catabolic expenditure. The changes observed with a deficiency or excess of iodine supply generally serve to maintain an adequate synthesis and supply of thyroid hormone, principally through modifications in thyroidal iodide accumulation and binding.

Starvation and Fasting
Multiple alterations in thyroid hormone regulation and metabolism have been noted during caloric restriction. The most dramatic effect is a decrease in the serum TT3 within 24-48 hours of the initiation of fasting 36-40b. Because changes in the free T3 fraction are usually small, the absolute concentration of FT3 is also reduced, clearly into the hypothyroid range. The marked reduction in serum T3 is caused by a reduction in its generation from T4 rather than by an acceleration in its metabolic clearance rate 41,42. The decline in T3 concentration is accompanied by a concomitant and reciprocal change in the concentration of total and free rT3. The increase in the serum rT3 concentration tends to begin later and to return to normal at the time serum T3 is being maintained at a low level with continuous calorie deprivation 38,39. Little change occurs in the concentrations of TT4 and FT4 and the production and metabolic clearance rates of T4 38,39,41,42. When small changes have been observed, they were generally in the direction of an increase in the FT4 concentration. They are attributed to decreased concentration of the carrier proteins in serum, as well as to their diminished association with the hormone caused by the inhibitory effect of free fatty acids (FFA) the level of which increases during fasting 40,43.

Decreased outer ring monodeiodination (5'-deiodinase activity) would explain both the decreased generation of T3 from T4 and the excess accumulation of rT3. This hypothesis seems to be fully supported by in vitro studies using liver tissue from fasted fats 44. It is further supported by the finding of increased generation and serum concentration of 3',5'-T2 and 3'-T1 and decreased 3,5-T2 and 3,3'-T2 44-47. However, a less important increase in the monodeiodination of the inner ring of T4 (5-deiodination) 42 explains the temporal dissociation of changes in serum T3 and rT3 concentration. A decrease in plasma T3 after fasting with an increase in hepatic type III deiodinase activity and mRNA has also been noted in chickens47a. An increase in the nondeiodinative pathway of T4 degradation with the formation of Tetrac has been also reported 48.

Considerable controversy remains regarding the mechanisms responsible for the observed changes in the rates of the deiodinative pathways of iodothyronines. Decreased generation of nonprotein sulfhydryls (NP-SH) as a cause of the reduction in 5'-deiodinase activity was suggested on the basis of the observed enhancement in enzyme activity by the in vitro addition of dithiothreitol. Reduced glutathione and NADPH had a similar effect 49. Although Chopra's 50 direct measurements of NP-SH in tissue during fasting seemed to confirm this hypothesis, the precise mechanism is likely more complex. Decreased tissue NP-SH content does not always correlate with the inhibition of T3 generation, which may be restored by glucose refeeding independently of changes in NP-SH content 50,51.

Composition of the diet rather than reduction in the total calorie intake seems to determine the occurrence of decreased T3 generation in peripheral tissues during food deprivation. The dietary content of carbohydrate appears to be the key ingredient since as little as 50 g glucose reverses toward normal the fast-induced changes in T3 and rT3 52. Replacement of dietary carbohydrate with fat results in changes typical of starvation 39,53. Refeeding of protein may partially improve the rate of T3 generation, but the protein may be acting as a source of glucose through gluconeogenesis 54. Yet, dietary glucose is not the sole agent responsible for all changes in iodothyronine metabolism associated with starvation. For example, the increase in serum rT3 concentration may not be solely dependent on carbohydrate deprivation since a pure protein diet partially restores the level of rT3 but not that of T3 39 (Figure 5-1). The composition of the antecedent diet also has an effect on the magnitude of the serum T3 fall during fasting 39,52. It is possible that the cytoplasmic redox state, measured in terms of the lactate/pyruvate ratio rather than glucose itself, regulates the rate of deiodinative pathways of iodothyronines 55.
Starvation produces a greater than 50% decrease in the maximal binding capacity of T3 to rat liver nuclear receptors within 48 hours 62. Although accompanied by a diminution of almost equal magnitude in the nuclear T3 content, it is unlikely that the observed change represents an alteration of the receptor content by the hormone as the more profound diminution of nuclear T3 content associated with hypothyroidism does not produce changes in the maximal binding capacity of T3 in rat liver nuclei. The reduction in maximal binding capacity has been demonstrated to coincide with a reduction in the level of the thyroid hormone receptors 62a. The affinity of the rat liver T3 receptor is not affected by starvation 62,63. Studies in humans have used circulating mononuclear cells and, probably due to the limited choice of tissue, results have been either equivocal or negative 64.

Other hormonal and metabolic changes during fasting may account for the observed alterations in the regulation and metabolism of thyroid hormones. Among them are the increase in plasma cortisol and suppression of adrenergic stimuli 65. Both changes are known to induce independently a decrease in the serum T3 concentration by inhibition of T4 to T3 conversion in peripheral tissues (see below). Accordingly, they may be partly responsible for the decrease in T3 neogenesis during starvation. There is likely a highly complex interplay between the changes in thyroid hormone and the many metabolic changes of starvation. In addition to a direct effect of glucose, changes in FFA, ketosis, and the redox state may influence thyroid hormone metabolism, while T3 itself may impact hepatic glucose production 40b.

Two major issues of theoretical and practical importance remain unresolved - do the observed changes in thyroid function produce some degree of hypothyroidism, and is this state beneficial to the energy-deprived organism? Although the suppressed serum TSH response to TRH suggests that the starving organism does not suffer from a significant deprivation in thyroid hormone, other observations indicate the contrary. The decreased pulse rate, systolic time interval, oxygen consumption, and decrease in activity of some liver enzymes are suggestive of hypothyroidism at the level of peripheral tissues 66. Furthermore, administration of T3 to restore its serum level to normal during fasting increased the production and excretion of urea and 3-methylhistidine 56,. Larger doses of T3, given during fasting, had even more profound effects. These effects included dramatic increased in the excretion of urea and creatine, and increased plasma levels of ketones and FFA indicating an accelerated protein and fat breakdown 68. Such evidence leaves little doubt that the decrease in T3 generation during calorie deprivation has an energy- and nitrogen-sparing effect. It is tempting to speculate that the result is beneficial in the adaptation to malnutrition through reduction in metabolic expenditure. Fasting is not only a useful model for studying the effects of calorie deprivation on thyroid hormone but is also the prototype of the "low T3 syndrome". 69 The latter is produced by a number of chemical agents and drugs, and accompanies a variety of nonthyroidal illnesses. It is possible that malnutrition, concomitant in a number of acute and chronic illnesses, is in part responsible for some of the observed changes in thyroid physiology.

Protein-Calorie Malnutrition (PCM)
As in the case of starvation, PCM is associated with a low serum T3 concentration and increased rT3 levels, probably due to similar changes in iodothyronine monodeiodination. However, important differences exist between the abnormalities in thyroid function observed in PCM and acute calorie deprivation. Most reports indicate important decreases in TBG and TTR concentrations, and there are also indications of hormone binding abnormalities 70,71. As a consequence, the free concentrations of both T4 and T3 are usually normal 70,72,72a. Recovery is associated with restoration of the level of serum thyroid hormones and binding proteins. Despite an accelerated turnover time, the absolute amount of extrathyroidal T4 disposed each day is reduced. Refeeding restores the T4 kinetics to normal 70. The thyroidal RAIU is reduced due to a defect in the iodine-concentrating mechanism 73. The most striking difference between starvation and PCM is the finding the latter of an exaggerated and sustained TSH response to TRH, with basal TSH levels either elevated or normal 70,72,72a,72b,74.

The experimental model of protein malnutrition in the rat yielded different results from those observed in humans. Serum T4 and T3 levels were found to be both elevated 75. However, in the lamb, as in humans, chronic malnutrition leads to a lower rate of T4 utilization 76.

Overfeeding and Obesity
Overfeeding produces an increase in the serum T3 concentration as a result of an increased conversion of T4 to T3. It is particularly marked when the excess calories are given in the form of carbohydrates 77. Thus, it appears that the effect of overnutrition on iodothyronine metabolism is the opposite of that of starvation. This finding gives further credence to the speculation that changes in thyroid hormone may serve to modulate the homeostasis of energy expenditure.

Although it has been reported that serum T3 concentrations correlate with body weight 78, it appears that this phenomenon reflects the effect of an increase in caloric intake on T3 production. Most studies find that obese subjects have normal thyroid function and hormone metabolism 79. Furthermore, no abnormalities in the hypothalamic-pituitary-thyroid axis have been demonstrated in obese subjects.

Minerals
Iodine. Of the many minerals that may affect thyroid function, iodine is the most important. It is an essential substrate for thyroid hormone synthesis and also interacts with the function of the thyroid gland at several levels.

Acute administration of increasing doses of iodide enhances total hormone synthesis until a critical level of intrathyroidal iodide is reached. Beyond this level, iodide organification and hormone synthesis are blocked (the acute Wolff-Chaikoff block). Chronic or repeated administration of moderate to large doses of iodine causes a decrease in iodide transport resulting in a decrease in its intrathyroidal concentration. The latter relieves the Wolff-Chaikoff block and is known as the escape or adaptation phenomenon. Although the exact mechanisms of the block and escape remain unknown, they appear to be autoregulatory in nature since they are independent of pituitary TSH secretion. Iodoloactones may play a role in the induction of the Wolff-Chaikoff block 80. One mechanism through which iodide acts is via desensitization of the thyroid gland to TSH. In TSH stimulated glands, iodine rapidly reduces the level of the mRNA for thyroid peroxidase (TPO) and the Na/I symporter (NIS) but not for thyroglobulin (Tg) or the TSH receptor (TSHr) 80a. Iodine also antagonizes TSH stimulated thyrocyte proliferation 80a. In FRTL-5 cells, iodine blocks the TSH stimulation of Tg synthesis but does not alter the level of the Tg mRNA 80b. These actions occur without a change in TSH receptor number, and may, in part, be via an action on adenylyl cyclase. More detailed description is provided in Chapter 2.

Another effect of large doses of iodine, apparently independent of TSH and hormone synthesis, is the prompt inhibition of hormone release. It has been exploited to achieve rapid amelioration of thyrotoxicosis in Graves' disease and toxic nodular goiters (see Chapters 11 and 13). In normal persons, the inhibitory effect of large doses of iodine on thyroid hormone release produces a transient decrease in the serum concentration of T4 and T3. It causes, in turn, a compensatory increase in serum TSH, which stimulates hormone secretion and thus counteracts the effect of iodine 81,82. The mechanisms of thyroidal autoregulation are believed to serve the purpose of accommodating wide and rapid fluctuations in iodine supply.

The most intriguing effects of iodine are the involution of hyperplasia and the decrease in vascularity that occur when the ion is administered to patients with diffuse toxic goiter. Iodine may be able to induce apoptosis in thyroid cells82a,82b. Under different circumstances, iodide may intensify the hyperplasia and produce a goiter (Chapter 20).

Iodine deficiency used to be the leading cause of goiter in the world and still remains so in certain regions. When severe, it can cause hypothyroidism and cretinism, described in detail in Chapter 20. In the United States and the rest of the developed world, untoward effects from excess iodine supplementation or the use of iodine-containing compounds are more common than problems related to iodine deficiency.

Excess iodine can be responsible for the development of goiter, hypothyroidism, and thyrotoxicosis. However, it should be emphasized that these complications usually occur in persons with underlying defects of thyroid function who are unable to utilize the normal adaptive mechanisms. Iodide-induced goiter (iodide goiter), without or with hypothyroidism (iodide myxedema), is encountered with greater frequency in patients with Hashimoto's thyroiditis or previously treated Graves' disease 83,84. Other predisposed persons include those who have undergone partial thyroid gland resection, patients with defects of hormonogenesis, and some with cystic fibrosis 85. Drugs such as phenazone 86,87, lithium 88, sulfadiazine 89, and cycloheximide 90 may act synergistically with iodide to induce goiter and/or hypothyroidism.

More rarely, ingestion of excess iodide may cause thyrotoxicosis (iodide-induced thyrotoxicosis or Jodbasedow) 90a. This was initially observed with the introduction of iodine prophylaxis in areas of endemic iodine deficiency 91,92. It has also been observed after the administration of iodide in excess to patients with nodular thyroid disease residing in areas of moderate iodine deficiency or even iodine sufficiency 93,94. Although the exact mechanism of induction of thyrotoxicosis remains obscure, it may be related to the stimulation of increased thyroid hormone synthesis in areas of the gland with autonomous nodular activity.

Ingestion of excess iodide by a gravid woman may cause an iodide goiter in the fetus, and if the gland is large enough it may result in asphyxia during the postnatal period (Chapter 20). Consumption of Kombu, the iodine-rich seaweed, is responsible for the occurrence of endemic goiter in the Japanese island of Hokkaido 95. It has also been suggested that the increase in dietary iodine content in the United States during the last three decades is responsible for the higher recurrence rate of thyrotoxicosis in patients previously treated with antithyroid drugs 96.

Calcium. Calcium is said to be goitrogenic when in the diet in excess. Administration of 2 g calcium per day was associated with decreased iodide clearance by the thyroid 97. The action is unknown, but it may in some way make overt a borderline dietary iodine deficiency. It has been recently shown that calcium reduces the absorption of thyroxine 97a.

Nitrate. Nitrate in the diet (0.3 - 0.9%) can interfere with 131I uptake in the thyroid of rats and sheep 98. This concentration is found in some types of hay and in silages.

Bromine. Bromine is concentrated by the thyroid and interferes with the thyroidal 131I uptake in animals 99,99a and humans, possibly by competitive inhibition of iodide transport into the gland. Bromine can also induce alterations in cellular architecture, blood supply and can lead to a reduction in T4 and T3 levels 99b.

Rubidium. Rubidium is goitrogenic in rats 100. However, the mechanism of action is unknown. Cobalt deficiency is associated with a reduction in type I monodeiodinase activity and a fall in T3105a while cobalt excess may produce goiter and decreased thyroid hormone production105b.

Florine. Fluorine is not concentrated by the thyroid but has a mild antithyroid effect, possibly by inhibiting the iodide transport process 101. In large amounts, it is goitrogenic in animals. The amounts of fluorine consumed in areas with endemic fluorosis are not sufficient to interfere with thyroid function or to produce goiter 102,103. However, other data suggest that dietary fluorine may exacerbate an iodine deficiency and thus modulate the distribution of goiter in areas with low iodine intake 104.

Cobalt. Cobalt inhibits iodide binding by the thyroid 105. The mechanism is unknown. It is sufficiently active to have been used in the treatment of thyrotoxicosis 106.

Cadmium. Administration of cadmium to rats or mice decreases serum levels of T4 and T3 106a,106b. It also decrease the activity of hepatic Type I - 5’Deiodinase 106a,106c.

Lithium Ion. Lithium ion is goitrogenic when used in the treatment of manic-depressive psychosis and can induce myxedema 107. Experimentally, lithium increases thyroid weight and slows thyroid iodine release 108. When lithium carbonate was given to human subjects in doses of 900 mg four times daily, there was a significant decrease in the rate of release of thyroidal iodine in euthyroid and hyperthyroid subjects 109. Lithium also decreases the rate of degradation of T4 in both hyperthyroid and euthyroid subjects 110. Inhibition of thyroid hormone release may be the dominant effect of the ion 110a. Therefore, the decrease in serum T3 concentration is greater in hyperthyroid patients, and changes in the rT3 level, if any, are minimal 111-113.

A number of mechanisms have been suggested for the effects of lithium. One well-documented phenomenon is a potentiation of an iodide-induced block of binding and hormone release 88,114, perhaps because lithium is concentrated by the thyroid 115 and increases the intrathyroidal iodide concentration 109,111 (Figure 5-2). Although it has been shown that lithium inhibits the adenylate cyclase activity in the thyroid gland as well as in other tissues 116, it also blocks the cAMP-mediated translocation of thyroid hormone. The latter effect, which is probably responsible for the inhibition of hormone release, appears to be due to the stabilization of thyroid microtubules promoted by lithium 117. In rat brain, lithium administration decreased both the levels of the Type II 5’Deiodinase and the Type III 5 Deiodinase 117a. In the rat, lithium may also lead to an alteration in the distribution of thyroid hormone receptors with the alpha 1 isoform being increased in the cortex and decreased in the hypothalamus while the beta isoform was also decreased in the hypothalamus117b.

An exaggerated response of TSH to TRH may be seen in a majority of lithium treated patients 110a but an elevated basal TSH is usually absent. An increase in the basal serum TSH concentration and its response to TRH most likely represents an early manifestation of hypothyroidism rather than a direct effect of lithium on the hypothalamic-pituitary axis 118. The prevalence of goiter has been reported to be as high as 60% 110a. Based on studies in FRTL-5 cells, lithium may have direct mitogenic effects on the thyroid that are independent of TSH and cAMP110b. The occurrence of hypothyroidism during lithium therapy occurs in 10-40% of lithium treated patients and is far more frequent in women than men110a,118a, 118b,118c.

Figure 5-2. The potassium perchlorate discharge test was carried out in a euthyroid patient during lithium treatment with serum lithium concentrations of 0.8 - 1.3 mEq/liter and during a period without lithium for 10 days. After the administration of radioiodide thyroidal isotope, content was measured for three hours before and 90 minutes after the administration of 200 mg perchlorate. The iodide perchlorate discharge test result was negative in patients not receiving lithium (B) but was strongly positive in patients under lithium (A) treatment. (From B.F. Andersen, Acta Endocrinol., 73: 35, 1973, with permission of the author and publisher)

Although much less frequent, lithium therapy has been associated with the development of thyrotoxicosis 110a. Lithium is also reported to produce exophthalamos during chronic therapy; the condition regresses when treatment is stopped. The phenomenon is a protrusion of the globe but does not involve the other changes of infiltrative ophthalmopathy of Graves' disease 118,119.

Selenium. Selenium is a component of the enzymes glutathione peroxidase (GSH-Px) and superoxide dismutase, both enzymes responsible for protection against free radicals. In addition, Type I 5’Deiodinase also contains selenium 119a. Thus, a deficiency of selenium could predispose the thyroid to oxidative injury and lead to decreased peripheral T3 production. In the elderly, reduced selenium levels have been associated with a decreased T3/T4 ratio 119b. It has been postulated that the combined deficiency of iodine and selenium in Zaire results in myxedematous rather than neurologic cretinism because the decrease in peripheral conversion to T3 results in greater delivery of T4 into the neonatal developing brain 119c. In rats, selenium deficiency led to a decrease in renal but not hepatic Type I 5’ Deiodinase activity and serum T3 levels were unaffected 119d. Selenium deficiency led to decrease GSH-Px activity in the liver, kidney and rbc’s but not the thyroid 119d. Serum T4 was normal when both dietary iodine and selenium were both deficient, but was reduced when either was deficient alone 119d. In other studies, brain GSH-Px and Type I deiodinase activity were normal in the presence of iodine or selenium deficiency while brain Type II Deiodinase activity was increased by iodine deficiency and unaffected by selenium deficiency 119e. In contrast in brown adipose tissue (BAT), both selenium and iodine deficiency led to decreased deiodinase activity and decreased production of the uncoupling protein 119e.

Treatment of goitrous children with combined seleium and iodine deficiency leads to a reduction in serum TSH and goiter size119f. The response, however, was correlated with the selenium level with both the goiter and TSH responses being correlated with the baseline selenium level 119f.

Physical and Emotional Stress
Perhaps the most dramatic study of emotional stress is that reported by Kracht 120, who found that stress provoked thyrotoxicosis in wild rabbits. Although some stress models may prompt secretion of thyroid hormone in animals 120,121, this effect is unlikely to occur in humans, at least for a sustained period of time. The stress-induced increase in adrenocortical activity tends not only to suppress TSH release but also to inhibit T3 production. A major problem in the analysis of available date is the difficulty in separating effects produced by non-specific stress from the effects caused by the agents used to induce the stress. Many of the changes in thyroid function described in this chapter under the headings starvation, temperature, altitude and anoxia may be due, in part, to stress.

Posted by: hardasnails1973

http://jap.physiology.org/cgi/conten.../88/5/1820#B17

THis tells all now how do I rest my self ?

Posted by: hardasnails1973

Dr. Just called
Told me I was a knuckle head for eating only 3000 caloires especially on the "supplments" Should have been excess of 4,000 caloires with my metabolism and with stress involved and basically starved my self into shut down. Will Do what every it takes to get me back on track. I meet with him monday 10 am..
Needs to rule out pituituary shutt down or thyroid

Posted by: Mudge

http://www.ncbi.nlm.nih.gov/entrez/q..._uids=12213860

You could try searching here, Nandi has probably picked through here on his own.

http://www.ncbi.nlm.nih.gov/entrez/q...arch&DB=pubmed

Posted by: hardasnails1973

since gh levels are ok and cortisols, I just hope that its only thyroid. My neck has gotten noticely thicker, voice more horse, and body is sucking up iodine like crazy, plus he suspects i may be anemic with low RBC, hemocrit. He told me this in less then 2 minutes

Posted by: chiquita6683

Im really sorry for all of my previous posts, and in .your journal, like how annoying am I

I was having a nervous breakdown there, not my brightest moment

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