Re: Lab Results/2nd Post

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

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.

February 25, 2005