Re: Questions about Armour

[Guest guest]

>>I know Armour PI says increase by

15mg every 2-3 weeks, can I go higher than that? And what level

should I shoot for before agreeing to another blood test? Should I

take part of it periodically during the day or all at once? Also,

can you explain the benefit of taking it sublingually?<<

It is best to increase SLOWLY, the 15MG every 2-3 weeks will get you there best!

There is no RIGHT level to shoot for except what is exactly right for YOU, where

you no longer have hypo symptoms but have no hyper symptoms either. That is

another reason to increase slowly, so you don;t accidentally overshoot YOUR

correct dosage. Armour should be taken at least twice a day, and some of us do

best on even more often, that is trial and error for what is best for you too,

but at least twice a day to start with. The benefit of sublingual is it is

directly absorbed into the bloodstream without interference from poor digestion

which is common in hypothyroidism, and less interference from what you have

eaten or will eat in the next couple hours as it is absorbed from the stomach.

*Artistic Grooming * Hurricane, WV

Fat cat? Diabetes? Listowner for overweight or hypothyroid cats

http://groups.yahoo.com/group/hypokitties/

[Guest guest]

>>I know Armour PI says increase by

15mg every 2-3 weeks, can I go higher than that? And what level

should I shoot for before agreeing to another blood test? Should I

take part of it periodically during the day or all at once? Also,

can you explain the benefit of taking it sublingually?<<

It is best to increase SLOWLY, the 15MG every 2-3 weeks will get you there best!

There is no RIGHT level to shoot for except what is exactly right for YOU, where

you no longer have hypo symptoms but have no hyper symptoms either. That is

another reason to increase slowly, so you don;t accidentally overshoot YOUR

correct dosage. Armour should be taken at least twice a day, and some of us do

best on even more often, that is trial and error for what is best for you too,

but at least twice a day to start with. The benefit of sublingual is it is

directly absorbed into the bloodstream without interference from poor digestion

which is common in hypothyroidism, and less interference from what you have

eaten or will eat in the next couple hours as it is absorbed from the stomach.

*Artistic Grooming * Hurricane, WV

Fat cat? Diabetes? Listowner for overweight or hypothyroid cats

http://groups.yahoo.com/group/hypokitties/

[Guest guest]

Just for your reference.

74 mcg of Synthroid is about equal to 1 grain of Armour.

So, you current one grain of Armour is less than your Synthroid dose.

115 mcg of Synthroid = 1-1/2 grains of Armour

125 mcg of Synthroid = 1-2/3 grains of Armour

You can increase as much as 1/2 of a grain at a time if you can

stand it and don't develope some low adrenal problems, which are

similar to hyper symtpoms.

Other information that you might find useful to know is that the

total daily output of the healthy thyroid is around 3 to 5 grains a

day. If you have no adrenal problems and no nutritional deficitncies

like anemia, you cannot overdose on any thyroid dose less than your

own healthy thyroid would make. The reason for this has to do with

the regulation of pituitary which works to prevent thyroid levels

from going too high.

So, if you take 1 grain of Armour, the pituitary will drop TSH by

the amount needed to tell your thyroid to drop it's production by

one grain or more keeping your daily total at or below 3 to 5 grains

or whatever it is you need.

A study done on healthy people found that the pituitary will zero

out thyroid doses less than 3 to 5 grains. In other words doses less

than 3 to 5 grains had absolutely no effect on the person due to the

pituitary working to keep things exactly the same in the blood.

Other studies have also shown that doses less than about a minimum

of 3 grains seem to have no effect on blood levels of thyroid. In

severly hypothyroid people, small doses of thyroid will have an

effect of raising the metabolic rate, but this does not mean it

makes them normal.

So, the vast majority of people will not see much benifit from

thyroid doses less than 3 grains. There are some lucky ones who can

get by on less. 3 grains is 220 mcg of Synthroid.

Doses of Synthroid as small as 50 mcg have been found to drop TSH

into the normal range, yet harldy any thyroid patient feels good at

this dose. Lots of studies have cast doubt on the usefullness of the

TSH test for treating thyroid patients and adjusting doses. It is

just not accurate.

http://www.thyroid-info.com/articles/david-derry.htm

http://www.suite101.com/article.cfm/graves_disease/98900

If you'd like to know a method youcan do on your own to adjust your

meds and to know how well you are doing, check out these pages:

http://www.drrind.com/tempgraph.asp

http://www.thyrophoenix.com/self_monitor.htm

Here are some articles that add to this:

http://thyroid.about.com/library/derry/bl11.htm

_____________________________

Statement from Dr. Derry in personal letter to a friend.

The statement by C.P. Lalonde in 1948 review: " When thyroxine is

administered to a thyroidectomized or myxedematous patient, it takes

250 -350 micrograms of thyroxine to maintain a normal metabolism.

( et al, 1935, Means, 1937) "

C. P. Leblond. Iodine metabolism. Advanc Biol Med Phys 1:353-386,

1948.

It does not say but I believe they gave it intravenously because it

is so badly absorbed orally. But IV thyroxine works well.

_____________________________

Author: Dr PBS Fowler

Date Published: 23-May-2001

Publication: Lancet 2001; 357: 619-24. Volume 357,

Number 9273 23 June 2001

Title: Letter in response to Colin Dayan's article '

Interpretation of thyroid function tests'.

Before the days of hormone assays, hypothyroid patients

received about double the average dose of thyroxine

given today, but did not develop osteoporosis or atrial

fibrillation. Doses should be judged clinically rather

than be governed by misinterpreted hormone results.

P B S Fowler

1 Dayan CM. Interpretation of thyroid function tests.

Lancet 2001; 357: 619-24.

__________________________________________________

Prognosis and treatment of COMMON THYROID DISEASES

Proceedings of a Symposium held in San Francisco,

California, U.S.A. - G March 1970

Editors : HERBERT A. SELENKOW AND FREDRIC HOFFMAN

When treatment of hypothyroidism is initiated in adults who have

been hypothyroid

for several months or longer, small doses of hormone are generally

used

to minimize the risk of cardiovascular complications.

The smallest dose of T4 which will

cowistently lower serum TSH has been 50 ug per day (0.05 mg). We

thus use this

dose of medication as initial treatment dose and maintain it for 10-

14 days. The

medication is then increased to 100 ug per day and kept there for a

month in

severely hypothyroid patients who are over 40 years of age. In

younger individuals,

more rapid increases may be used.

Desiccated thyroid was a relatively

reliable and very useful treatment for many years. During the past

decade a number

of reports appeared indicating that some preparations of desiccated

thyroid might

contain lowered activity or be inactive ( e t al., 1963;

Brauerman and

Ingbar, 1964; Catz et a].. 1962; Modell, 1964; Bartuska et dl.,

1966). Such

inactivity was considered to be due to one of the following causes:

(I) deterioration

of the drug on the pharmacy shelf, (2) batches of dry gland of low

initial

biological potency, or (3) failure of absorption of the densely

packed tablets

(Bartuska et dl., 1966).

Since the serum levels of T3 are nearly

unmeasurable, reproduction of the metabolic effects of the two

hormones with

T4 alone results in a higher serum T4 concentration than exists in

the normal subject.

T3 also has been used as replacement therapy for hypothyroidism. It

is loosely

bound to thyroxine-binding proteins in blood and has a shorter half-

life.

Thus, in the average patient requiring 280 ug T4 daily,

190 ug are absorbed. Of this, 90-100 ug replaces the T4 normally

secreted daily

and the remainder provides the physiological equivalent of normal T3

secretion.

Objective and accurate assessment of adequate replacement dosage

with thyroid

hormone is difficult. The clinical impression provided by history is

usually not an

entirely accurate indicator, since relief of the profound symptoms

of hypothyroidism

produced by tiny doses of thyroid medications may be dramatic.

Physical

examination is helpful, but it is often not possible by this means

to distinguish a

minimally hypothyroid individual from a euthyroid one. Moreover, the

range of

thyroxine concentrations in normal subjects is wide and varies with

age (Oddie

and Fisher, 1967) and sex (Oddie et al., 1966). It is difficult to

assess what is the

optimal dose for any one subject, for at present we have no

objective, easily

quantifiable parameter to assess response of body tissues to thyroid

hormone

replacement. Measurements of serum TSH, kinetics of reflex time, and

oxygen

consumption are helpful, but not entirely reliable for this purpose.

SELENKOW: I primarily follow my patients clinically. The laboratory

tests are

most useful in confirming euthyroidism once the maintenance dosage

of thyroid

has been attained.

SELENKOW: ...if the patient is only on

one of the commercial sodium levothyroxine preparations (either

Synthroid or

Letter), the free thyroxine index is also not applicable.

Individuals on physiological

replacement doses of pure sodium levothyroxine have elevated levels

(high normal

to hyperthyroid range) of serum thyroxine (-Pattee). The resin

uptake

tests in these persons are also elevated above normal, so that in

patients on 300

or 400 pg of sodium levothyroxine a day, the PBI or serum thyroxine

level will

be in the high range and so will the free thyroxine index.

On physiological doses of desiccated thyroid, USP or on Liotrix

(Euthroid,

Warner-Chilcott) the serum levels of all thyroid function tests will

more closely

relate to what you expect in a normal euthyroid person.

BURKE: I will not repeat the truism that the most reliable index of

response to

therapy is the clinical status of the patient, but this really

should be emphasized,...

BECKER: I would like to emphasize what Dr. Odell has said. I believe

that the

physician must pay close attention to the patient.

GREENSPAN: Dr. Becker, you have done a noble job in resurrecting the

ghost of

the BMR. One of the big problems in measuring the tissue effect of

T4 is that we

really do not know the exact mechanism of action of thyroxine.

Overall oxygen

consumption must be really a very late effect of high levels of

circulating thyroxine.

If we had some way of measuring more precisely the effect of

thyroxine on a

specific tissue, we would have a better and more precise method for

measuring its

tissue effects.

A dose of T4 of about 20 ug/kg body weight will usually produce good

results in newborns. It is not necessary to initiate treatment with

small doses as is

done in adults. Circulating thyroxine should be measured

periodically and in infants

and small children should be maintained at 9-15 ug/100 ml (as

thyroxine

iodide 6-10 ug %). In addition, growth rate and bone age should be

followed

serially. Inadequate replacement will result in slowing of growth

rate and delay in

bone maturation.

_____________________

http://thyroid.about.com/library/derry/bl3a.htm

Dr. Derry

Chronic fatigue symptoms of low temperatures, fatigue and

accompanying brain fog are classical signs and symptoms of

hypothyroidism. (1-3) There are many psychological symptoms and

personality difficulties which accompany brain dysfunction related

to hypothyroidism many of which have been published in a classical

1958 publication. (3) One of the most prominent is loss of self-

esteem and inability to cope properly.

The doses a patient gets when monitored by the TSH is currently two

thirds or less of the well established clinically effective doses

established from 83 years of clinical experience before the TSH

arrived. (5-6)

ff and LoPresti (7) discussed this problem in their

conclusions:

" It may be that the critical events controlling thyroid hormone

action in non-thyroidal illness (all illness not related to thyroid)

are largely regulated at the cellular level and that we are naive to

believe that we can make interpretations from circulating thyroid

hormones values. " (7)

So the human body can operate at all the different levels of thyroid

hormone. But at the low levels function is poor. At the correct

levels the patient copes well and does well.

Repeatedly, studies on normal people with increasing doses of

thyroid found humans have a wide range of tolerance for thyroid

hormone (8-11). All body tissues, including the brain can adapt

individually to the higher or lower levels of thyroid hormone

Because all organs can adapt to many levels of thyroid hormone it

suggests that for each person there is an individual level at which

this person can cope and function at optimal levels. (5)

For example, in a sixteen part study of the effects of desiccated

thyroid on healthy prisoners Danowski et al found they tolerated

dosages of 9 grains of desiccated thyroid (540 mgs which equals

about 540 micrograms thyroxine) without ill effects. (9-11). On

studies on obesity and thyroid hormone where the dosages for three

months were between three grains and 25 grains (1500 mg of

desiccated thyroid equals about 1500 micrograms of Eltroxine) (12).

they said: " As in previous studies, these dosages of desiccated

thyroid were well tolerated by the subjects. Occasional nervousness,

increased sweating, and decreased endurance were reported.

Tachycardia and slight increase in the systolic blood pressure and

decreases in the diastolic blood pressure appeared in all.

Electrocardiogram changes were minimal. Body weight decreased by an

average of 26 pounds during the 22 weeks of treatment. " (7).

________________________

[study of hormone replacement therapy following total thyroidectomy

in thyroid cancer--with special reference to the analysis of thyroid

hormone peripheral effects, using indirect calorimetry]

[Article in Japanese]

Nozaki H, Funahashi H, Sato Y, Imai T, Oike E, Kato M, Takagi H.

Second Department of Surgery, Nagoya University School of Medicine,

Japan.

Five weeks after the beginning of hormone replacement, T4 and free

T4 were slightly within range, and no enhancement of energy

metabolism was noted. From these findings, the post-operative TSH

suppression therapy carried out at our department is considered to

be justifiable also from the viewpoint of energy metabolism.

(dangers of long lasting low energy states from inadequate thyroid -

body does not respond to treatment after it has been hypo for too

long.)

__________________________

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.

________________________

http://www.drlowe.com/QandA/askdrlowe/armourthyroid.htm

That optimal dosage range is highly individual, but historically,

the typical patient's therapeutic window has been somewhere between

120 to 240 mg (2 to 4 grains). There's no way to accurately predict

what your therapeutic window is.

_____________________

Dr. Derry, " Breast Cancer and Iodine " :

Before the 1973-1974 change in laboratory diagnosis, the objective

of treatment in all cases was raise the thyroid dose up untill the

patient was in a state of well-being.

Before the 1973-74 change, the normal dose of thyroid was three

times the level seen now (2 -3 grains now) and there were no cases

of fractures or osteoporosis ever reported in the previous 80 years.

_________________________________

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.

______________________________

MINI REVIEW

Intrinsic imperfections of endocrine replacement therapy

J A Romijn, J WA Smit and S W J Lamberts

Department of Endocrinology, Leiden University Medical Center,

Leiden and Department of Internal Medicine, Erasmus Medical Center,

Rotterdam University, Rotterdam, The Netherlands

(Correspondence should be addressed to J A Romijn; Email:

j.a.romijn@...)

However, many patients

treated for endocrine insufficiencies still suffer from more or less

vague complaints and a decreased

quality of life. It is likely that these complaints are, at least in

part, caused by intrinsic imperfections

of hormone replacement strategies in mimicking normal hormone

secretion.

......effects of

hormones in general, and thus of hormone replacement strategies in

particular, are difficult to

quantify at the tissue level. Therefore, in clinical practice we

rely mostly on plasma variables –

`plasma endocrinology' – which are a poor reflection of hormone

action at the tissue level.

Complaints of thyroid patients....They range from

musculoskeletal complaints, to vague feelings of being

unwell, and to depression. Two approaches have been

used to decrease the complaints experienced by these

patients: an increase in the dose of L-thyroxine, and

combination treatment of thyroxine with tri-iodothyronine.

In some of the patients, a decrease in complaints

can be achieved by increasing the dose of thyroxine

above that required to restore TSH concentrations to

normal (1). For this reason, such patients are often

allowed to take a dose of thyroxine that would be

judged as overtreatment with respect to TSH concentrations.

The second approach was evaluated by

Bunevicius et al. (2), who performed a randomised controlled

trial to compare the effects of thyroxine alone

with those of thyroxine plus tri-iodothyronine. Patients

with hypothyroidism benefitted when 12.5 mg triiodothyronine

was substituted for 50 mg thyroxine in

their treatment regimens. This resulted in improved

neuropsychological functioning. Pulse rates and

serum sex hormone-binding globulin concentrations

were greater after treatment with thyroxine plus

tri-iodothyronine, indicating a slightly greater effect

on the heart and liver. Serum thyroxine concentrations

were lower and tri-iodothyronine concentrations

were greater after treatment with thyroxine plus

tri-iodothyronine, but serum TSH concentrations, a

sensitive measure of thyroid hormone action, were

similar after the two treatments. It should be noted

that not all patients benefitted from this approach

because, even in the group with combination therapy,

patients continued to report complaints of depression.

Thyroxine:

The thyroid secretes tri-iodothyronine (T3) (,20%) in addition to

thyroxine (T4) (,80%). In the absence of

thyroid function, exogenous thyroxine is not able to normalise the

concentrations of T4 and T3 in all tissues in rodents, even in the

presence of normal TSH concentrations. Despite this knowledge,

currently available preparations of T3 have unfavourable

pharmacological profiles and adequate markers of biological effect

are lacking. Additional evidence is required before combination

therapy can be advised.

First, it is remarkable that the normal values

of TSH show a more than tenfold variation, between

0.4 and 4.5mU/l. Because, in clinical practice, the optimal

TSH concentration for individual patients within

this range is unknown, titration of the substitution

dose of thyroxine within this tenfold variation is

relatively crude. Secondly, the intrinsic assumption of

many doctors in this approach is that normal TSH

concentrations reflect adequate thyroid hormone

concentrations, not only at the tissue level of the

hypothalamus and the pituitary, but also in the other

tissues. However, it is likely that this assumption is

erroneous, because TSH is produced only by the

pituitary gland and therefore may not reflect thyroid

hormone status in tissues outside the hypothalamo–

pituitary axis. This notion is supported by data obtained

from animal experiments.

Thyroxine is considered to be an

inactive hormone, because a thyroxine-specific receptor

has not been identified. Rather, thyroxine serves as a

prohormone, because it is the precursor of tri-iodothyronine.

Some tissues, such as muscle, have a relatively low

deiodinase activity and are dependent, to a great

extent, on tri-iodothyronine derived from the thyroid

and the liver.

In rodents, it has been clearly demonstrated that

there is no single dose of thyroxine or tri-iodothyronine

that normalises thyroid hormone concentrations in all

tissues simultaneously in hypothyroid animals (3).

Therefore, it is highly likely that, in patients treated

with L-thyroxine, subtle derangements at the tissue

level are present with respect to thyroid hormone availability,

and probably also thyroid hormone action.

_______________________

A very good article by Dr. Lowe stating that some patients,

especially those with auto-immune thyroid disease need TSH

suppressive (high) doses of thyroid hormone to have good health.

http://www.drlowe.com/frf/t4replacement/intro.htm

The most effective of these therapies involves adjusting patients'

dosages of combined T4/T3 or T3 alone according to several indices

other than TSH and thyroid hormone levels. Those indices are signs,

symptoms, and various objective measures of tissue response to

particular dosages. When patients' dosages are titrated according to

these indices, dosages that prove safe and effective are typically

TSH-suppressive.[44] Evidence is available that this therapeutic

approach relieves patients' signs, symptoms, and measurable tissue

abnormalities such as low resting metabolic rates (RMR) according to

indirect calorimetry.

This observation suggests that dosages higher than those dictated by

the replacement concept more effectively relieve patients'

hypothyroid symptoms. Other research has shown that patients report

feeling better with TSH-suppressive dosages of thyroid hormone.[23]

[24][25] Moreover, psychiatrists report that dosages of T3 higher

than replacement dosages augment the depression-relieving effects of

antidepressants.[9][28][29][30][31][34] In addition, in a study of

patients made hypothyroid by therapeutic destruction of the thyroid

gland, some used TSH-suppressive dosages of thyroid hormone and

others used T4-replacement. Those on TSH-suppressive dosages didn't

gain excess weight; those on T4-replacement did. The researchers

concluded that T4-replacement was the cause of the excess weight

gain.[55] These published reports are consistent with thousands of

cases in which hypothyroid patients recovered from their symptoms

and other health problems with TSH-suppressive dosages of thyroid

hormone after T4-replacement failed to help them.

Kaplan's observation also suggests another point: that T4-

replacement keeps many hypothyroid patients' dosages too low to

relieve their symptoms is an indictment of the concept of

replacement. As the cause of

(1) the continued suffering and debility of patients,

(2) an increased incidence of potentially life-threatening diseases,

and

(3) the need for the chronic use of medications,

___________________________

Dr. Derry article:

http://thyroid.about.com/library/derry/bl11.htm

The effective dose physicians used by clinical judgment and

experience before 1975 was around 2-3 times higher than the dose

used by TSH blood test monitoring. So everyone's dose of thyroid

after 1975 was decreased by about two thirds of well established

clinically effective doses.

***********************

Another Derry article:

http://thyroid.about.com/library/derry/bl4a.htm

In the 1960s it was textbook material after 70 years of experience

using thyroid that a dose below 180 mg of desiccated thyroid (3

grains) could not be measured clinically or in the laboratory. In

other words it was without effect.(2) The approximate equivalent

dose of synthroid or thyroxine (T4) would be about 180 micrograms.

(3)

So unless your dose is above 180 there is little chance of regaining

your hair back and the problem likely continue and get worse. You

can tell when you are approaching the right dose personally when the

itching starts to go away permanently. Depending on how old you are

and other medical history it is likely though you would get complete

relief with a dosage up around 200 micrograms of Synthroid or

higher. We know that there are no side effects at those dosages.

Dosages of thyroxine (Synthroid, T4) of up to 300 micrograms are

without morbidity or mortality. (no sickness or deaths) (4)

_____________________________

Dr. Lowe's wife:

http://www.drlowe.com/emailnewsletter/2003archive.htm

Instead, they adjust dosages according to how patients respond to a

particular dose. As studies have shown, this approach produces far

superior treatment results than does adjusting dosages according to

thyroid test results.[1][2]

________________________

Dr. Lowe uses this guide:

http://www.drlowe.com/clincare/clinicalforms/areyouoverstimulated.pdf

to determine if the patient is on too high a dose. In other words,

they raise thyroid dose up untill the patient feels best and use

this form as a way to make sure they haven't gone too high. Dose is

determined purely by how the patient feels and no tests are used

_____________________

(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.

[Guest guest]

Thanks to all for the valuable information - I'll start taking the

Armour sublingually, and try to convince the doctor that I know what

I'm doing (with everyone's help) so he'll let me increase the dosage

on my own until I feel better. Unfortunately at the rate of 15mg

every 3 weeks, I'm going to feel pretty bad for a while, I just hope

it's worth it in the long run!

Thanks everyone - I'll let u know how it goes - I can always find

another doctor, right?

Joyce

>

> > 115 mcg of Synthroid = 1-1/2 grains of Armour

> > 125 mcg of Synthroid = 1-2/3 grains of Armour

>

> I wanted to also squeeze myself in here and tell you that though

> Tish put the conversion amounts above, you will need much more of

> Armour than the above to rid yourself of symptoms...as she later

> talks about. I was on .125 Synthroid, and my optimal dose ended up

> being 3 grains.........and I am now on 3 1/4 grains.

>

> Janie

[Guest guest]

Thanks to all for the valuable information - I'll start taking the

Armour sublingually, and try to convince the doctor that I know what

I'm doing (with everyone's help) so he'll let me increase the dosage

on my own until I feel better. Unfortunately at the rate of 15mg

every 3 weeks, I'm going to feel pretty bad for a while, I just hope

it's worth it in the long run!

Thanks everyone - I'll let u know how it goes - I can always find

another doctor, right?

Joyce

>

> > 115 mcg of Synthroid = 1-1/2 grains of Armour

> > 125 mcg of Synthroid = 1-2/3 grains of Armour

>

> I wanted to also squeeze myself in here and tell you that though

> Tish put the conversion amounts above, you will need much more of

> Armour than the above to rid yourself of symptoms...as she later

> talks about. I was on .125 Synthroid, and my optimal dose ended up

> being 3 grains.........and I am now on 3 1/4 grains.

>

> Janie