Re: TSH

[Guest guest]

HI Debbie, I am no expert yet I do know that any doc that really understands

the thyroid and it's function and how to treat it....just " glances " at the TSH.

Because the best way to " doctor " your hypo symptoms is by your symptoms...not

the TSH. By suppressing your TSH (getting it as low as possible) your hypo

symptoms and life of hell on earth will go away. It has been proven over and

over by women just like myself that the TSH HAS to be on the low side and the T3

on the very high side.

The tests that the regular medical profession uses are wrong wrong wrong. It

should go back to the way it used to be when a doc used temp and symptoms to

take care of their patients...this was tried and true and worked very well until

some smarty pants came along and decided there had to be " normal limits " and new

testings. Since then many many women are suffering needlessly. I was told that

Epstein Barr and all the diseases that leave people suffering with out a cure

are because of the TSH and T4 protocol. These two tests MISS SO MUCH and any

doc that only uses those two tests as a base line of testing doesn't have a clue

as to what they are doing. If your doc gives you grief over increasing your

Armour and getting yoiur TSH suppressed and your T3's in the higher range...a

new doc is in order ASAP. He/She isn't caring how you are feeling or healing,

all he or she cares about at this point is being correct!!

Aren't you seeing Doc Milton at the end of the month? He will take such good

care of you...you won't have any worries, concerns or questions once he is

treating you hun

Hugs...PattiSue

TSH

I thought my doc appointment was yesterday and posed this question in

the early morning. But then found out it is tomorrow, so I'm asking

again. Guess nobody answered b/c by the time they read it they assumed

it was too late.

Anyway, tomorrow I'm going to tell my doc that I want my armour

increased gradually until my FT3 is in the high range even if the TSH

gets really low.

Please, somebody tell me the reasoning behind the TSH getting really

low, but it not mattering anyway. I did find in my stuff that there

should be no concern for this as they give high doses of T3 to arrest

thyroid cancer and these people don't get hyper. But seems like there

was something else that I can't remember. I want to be sure to say the

right thing.

Blessings,

Debbie K.

[Guest guest]

Here's some more info from Domissee that has more info than you

need, but will help:

MS: What are your thoughts about the use of the TSH test and

its " normal range " as a primary means of diagnosis of hypothyroidism?

JD: Not much. 2 reasons: (1) The TSH is an indirect measure of the

height of thyroid hormone function and is influenced by many factors

in addition to the height of the free-T4 and free-T3 serum levels.

Endocrinologists are confusing the great sensitivity of the test

(for measuring the height of the thyroid stimulating hormone serum

level) with the idea that it is therefore the most accurate and

appropriate measure of T4 and T3 thyroid hormone function, which it

is not - the free-T4 and free-T3 serum levels are the best arbiters

of that! They are still 'stuck' in the time when the Total-T4 and

Total-T3 (and other even-less-accurate measures) were the only

measures available. They have not adapted to the paradigm-shift in

accuracy of the free-levels. Besides, an elevated TSH can only

suggest primary hypothyroidism (in which the defect is in the

thyroid gland itself), not secondary, tertiary or nonthyroidal-

illness hypothyroidism (in which the defect is in the pituitary,

hypothalamus, and peripheral enzymatic conversion of T4-to-T3 with

5'deiodinase, respectively, and TSH is not elevated in these types

of hypothyroidism, may even be below its 'normal range'). If the TSH

has any usefulness at all, it only has it in a trio of tests

including the FT4 and FT3 as well. There are many circumstances in

which one can dispense with the TSH test, but never, in my opinion,

with the FT4 and FT3 levels.

(2) The so-called 'normal range' is way too high. Even in

conventional circles it has become acceptable to make a diagnosis of

grade-3 hypothyroidism (the mildest grade) when the TSH level is " in

the upper half of its 'normal range' " (above 2.0, rather than 4.0 or

5.0 mIU), although very few conventional physicians will do this, or

treat this 'mild, sub-subclinical' degree of hypothyroidism. But

isn't that strange? Doesn't that immediately render the TSH normal

range cut in half, to a new normal range of 0.4-2.0? For several

years I adhered to the grade-3 primary hypothyroidism range, with

2.0 as my cut-off point. But, eventually, I ran into too many

patients who had classic hypothyroid symptoms, which cleared

completely on appropriate thyroid treatment, and whose TSH was below

2.0 (but above 1.5) and with FT4 and FT3 levels in the low ends of

their 'normal ranges'. So I lowered my range to 0.2-1.5. For several

months I was happy to be helping more people (those whose TSH fell

between 1.5 and 2.0). Finally, I found some patients with several

symptoms and signs of hypothyroidism whose TSH was between 1.0-1.5;

so I lowered my range, for the last time, to 0.1-1.0; I now treat

primary hypothyroidism with a TSH of >1.0 (if the FT4 and FT3 are

low-normal, not above the middle of their 'normal ranges'). Some

physicians are still waiting for the TSH to go above 6.0 or even

10.0 mIU before they'll agree that the patient's hypothyroidism

needs treatment!

[Guest guest]

(Again, more info than you may need, but excellent to know:)

Almost every conventional discussion of thyroid disease focuses on

the use of the Thyroid Stimulating Hormone (TSH) as the

diagnostic " gold standard " for thyroid disease. The TSH is used

almost exclusively by most conventional physicians as the means of

diagnosing thyroid disease, irrespective of symptoms. Typically, if

the TSH level is above the normal range, a patient is diagnosed as

hypothyroid, and TSH levels below normal range are interpreted as

hyperthyroidism. But is the TSH test and the reference " normal

range " accurate? Should thyroid disease diagnosis be based primarily

on this one test? Some experts say no.

Dr. A P Weetman, professor of medicine, wrote in the

article " Fortnightly review: Hypothyroidism: screening and

subclinical disease, " which appeared in the 19 April 1997 issue of

the British Medical Journal, the following groundbreaking statement:

" . . . even within the reference range of around 0.5-4.5 mU/l, a

high thyroid stimulating hormone concentration (>2 mU/l) was

associated with an increased risk of future hypothyroidism. The

simplest explanation is that thyroid disease is so common that many

people predisposed to thyroid failure are included in a laboratory's

reference population, which raises the question whether thyroxine

replacement is adequate in patients with thyroid stimulating hormone

levels above 2 mU/l. "

In response to Dr. Weetman, Derry M.D., Ph.D., a thyroid

expert and researcher, based in , British Columbia,

responded, saying:

" Why are we following a test which has no correlation with clinical

presentation? The thyroidologists by consensus have decided that

this test is the most useful for following treatment when in fact it

is unrelated to how the patient feels. The consequences of this have

been horrendous. Six years after their consensus decision Chronic

fatigue and Fibromyalgia appeared. These are both hypothyroid

conditions. But because their TSH was normal they have not been

treated. The TSH needs to be scrapped and medical students taught

again how to clinically recognize low thyroid conditions. "

This provocative response was how Dr. Derry came to the attention of

many thyroid patients, and interviewer Shomon, About's thyroid

guide. In this interview, Dr. Derry shares his fascinating and

innovative ideas about why he believes the TSH test needs to be

abandoned. This interview was conducted in July of 2000.

Shomon: First, Dr. Derry, can you tell us a little bit about

your medical background, and interest in thyroid testing and

treatment?

Derry: I have always been interested in Medical research. I

graduated with a Medical Degree from the University of British

Columbia, Canada in Vancouver in 1962. I interned at the Toronto

General Hospital. From there I went to McGill University and went

into a four year program to get my PhD in biochemistry and more

specifically in Neurochemistry at the institute set up by Wilder

Penfield called the Montreal Neurological Institute in Montreal. In

1967 I graduated with a PhD in biochemistry from McGill. I was hired

by the department of Pharmacology at the University of Toronto

Medical School as an assistant professor. For five years I did basic

biochemical research and taught medical students, dentistry students

and pharmacy students. Not long after I arrived in Toronto I was

became a Scholar of the Medical Research Council of Canada. That is

to say, my salary was paid by The Medical Research Council of Canada

to do pure research for five years. At the same time I worked week-

ends in charge and the only physician in a large 900 bed psychiatric

hospital called the Lakeshore Psychiatric Hospital. Meanwhile about

then (1970 ) I had a rearrangement of my domestic status. I ended up

marrying my present wife and by this gained three more children. I

had two of my own. All children were between 4 and 9 years old.

There was no way that the salary of an assistant professor in

Pharmacology at the University of Toronto was going to be able to

pay to raise five small children. After the legal aspects had been

settled my wife and I, the five children and a large Labrador

retriever boarded a 747 for British Columbia. Within two

weeks I started a general practice.

When I came back into General Practice I had in mind a saying I

attribute to Dr. Wilder Penfield which was (paraphrasing) " If you

listen to a patient carefully the patient will tell you the

diagnosis and if you listen even more carefully they will tell you

the most appropriate treatment " . Before I went back into practice I

had taken courses in interpersonal relationships and how to

communicate and listen better. Since I entered General Practice I

have taken more courses in personal development. My idea was to

learn more and more how to listen carefully and how to get my

personality (ego) out of the way of the conversation with the

patient. Because I was armed with this approach I developed, I have

been able to learn much in the last 28 years in practice.

After about 3-4 years in practice I thought I would start to do my

own research. I started with Vitamins. Amongst many other topics, I

taught Vitamins at the University of Toronto and when Dr. Linus

ing's book on Vitamin C and Cancer came out in 1970 I was asked

by the Faculty of Medicine to present the essential material of the

book to about 300 faculty members and students. Therefore, vitamins,

their prophylactic and therapeutic use was a good place for me to

start to investigate. So I investigated the use of vitamins for all

manner of disease. Eventually after about 10 years I had fairly well

exhausted every aspect of the therapeutic use of vitamins I could

think of. By then I knew what you could do and couldn't do with

vitamins. Most of the patients were only too glad to help me with

this and the ones who got better were very grateful. Since then I

have slowly over the last 15-20 years developed an interest in

thyroid problems. There are reasons for my interest in thyroid that

are too long to tell. Gradually I obtained copies of all the

relevant thyroid literature back to the 1883 Committee on Myxedema.

I have a huge library on the thyroid literature consisting of about

5000 reprints and books. All of the old textbooks I copied and have

them in my library for my use. All of this is computerized of

course. There are other aspects of my medical and biological

training in my CV. (See Dr. Derry's Biographical Information and

Chronological Curriculum Vitae

The consensus of thyroidologists decided in 1973 that the TSH was

the blood test they had been looking for all through the years. This

was about two years after I started practice. Having been taught how

to diagnose hypothyroid conditions clinically I was in a position to

watch to see what the relation of the TSH was to the onset of

hypothyroidism. What I found was many people would develop classic

signs and symptoms of hypothyroidism but the TSH was ever so slow to

become abnormal, rise and confirm the clinical diagnosis. Sometimes

it never did. Finally I began treat patients with thyroid in the

normal manner I was taught. I could not see why I had to wait for

the TSH to rise for me to be able to treat them.

The main ingredient of thyroid hormone, which distinguishes it from

other molecules of similar size (molecular size), was the element

which made thyroid hormone namely iodine. So I did a thorough search

of the literature on iodine. This review led me to try to use iodine

and thyroid therapeutically. The TSH had caused all research on the

therapeutic use of both of these substances to stop dead. My

biochemical and pharmacological background has allowed me to search

in areas of the literature that are impossible for a normal

physician or even a specialist to explore.

If you remember it was a long time before the medical profession

admitted that there were two new diseases to appear in the world

that were not there before. Chronic fatigue and fibromyalgia were

non-existent before 1980. This is seven years after the 1973

consensus meeting. So where did these two new diseases come from?

The symptoms and signs of chronic fatigue and fibromyalgia were

described in the literature in the 1930's as one way that low

thyroid could be expressed. Treated early it was easily fixed with

thyroid in adequate doses. But even then the clinicians had noticed

that if a patient has low thyroid (chronic fatigue and fibromyalgia)

for too long then it became more difficult to reverse all signs and

symptoms regardless of what they were.

Shomon: Why do you think that thyroidologists have decided that

the TSH test is the most useful -- or in many cases - the only test

for thyroid problems, versus a patient's clinical symptoms? How do

you think this has come to be considered the " gold standard " for

thyroid diagnosis and management?

Derry: The thyroidologists have been looking for a reliable

test for thyroid function since the beginning of the century. The

first important ones were the Basal Metabolic Rate, the cholesterol

and the creatine phosphokinase. (CK) . These were used mainly up to

about 1960. If you had a high cholesterol in the first half of the

century you got thyroid to lower it to normal. Details of using this

method of treatment were still described in the 1950's. The Basal

Metabolic rate became the fad in the 30s and 40s and almost every

office had a machine to measure it. It was quite good but subject to

difficulties of interpretation and interference by emotional

factors. However it still remains the only test that actually

measures the effects of thyroid medication on the human body. In the

1940's radioactive iodine became available from the Tennessee Valley

Atomic Energy Complex. Hence the metabolism of iodine could be

studied more closely. The radioactive iodine uptake by the thyroid

became a frequently used test, which was said to be infallible like

all the others when they first arrived. Every time there was a new

test it was declared to be reliable for telling if a person was

hyperthyroid or hypothyroid, but as with every previous test it

turned out to not be clinically applicable in all cases. In the

1960's when I was studying medicine the PBI (Protein bound iodine)

was heralded as the only test necessary, when it was low you had

hypothyroidism and when it was high you had hyperthyroidism. This

was written in some of the textbooks of the time. Eventually this

test went the way of the rest -- useful sometimes-- but doesn't

always agree with the clinical findings.

Next came the T4 or total thyroxine in the blood that is the free

and the protein bound thyroxine measured together. This was also

hailed as far superior to the PBI, but it too went the way of the

rest of the tests --as not being reliable enough. Finally the TSH

arrived in the late 60s and was boasted about as the final answer.

The TSH was not only able to deliver all the thyroid diagnoses but

it could be used as well for monitoring therapy. Over the following

twenty years the TSH was made more and more sensitive and because of

these improvements it was even more thought that it was the total

answer for thyroid diagnosis and treatment. However as the TSH was

so sensitive to orally-given thyroid hormone it meant literally

everyone was going to end up with a low dose by comparison with

previous doses. The new doses were about a third of the dose that

had been found to be clinically effective for every patient for

eighty years prior to the TSH.

The TSH had a ring of scientific rigor for those who have a

smattering of knowledge about thyroid metabolism. It was part of the

pituitary feed back mechanism for monitoring the output of the

thyroid gland. There is no doubt that it does accomplish this job.

But unfortunately the TSH value has no clinical correlation except

at absolute extremes with the clinical signs or symptoms of the

patient. The reasons for this are complex and I only want to discuss

one aspect but there are other important factors.

To start with the thyroid metabolism is controlled locally in the

tissue by each organ. That is the brain has one mechanism for

controlling the amount of thyroid available to the brain but it is

different from other tissues such as the liver. There are many

mechanisms by which each tissue controls the amount of thyroid

hormone which gets into the tissues. But to discuss one: there is an

enzyme in the tissue which deiodinates (takes one iodine off the

thyroxine T4) and makes T3 or triiodothyronine. These enzymes are

called deiodinases. Every tissue has different types of deiodinases.

To just give you one example: If you starve animals and study the

deiodinases in the brain and liver you find that the activity in of

the brain deiodinases go up by 10 times while at the same time the

liver deiodinases go down--not up. This mechanism is obviously meant

to preserve the functioning of the brain under starvation conditions

and not metabolize too much thyroid hormone in the liver. Therefore

the control of thyroid metabolism is in every individual tissue. The

problem with this is-- if a tissue needs more (such as the brain

with depression) there is no way for the brain to signal the thyroid

that it needs more sent up to it. The thyroid merrily goes on

putting out the same amount of thyroid hormone. So the patient can

have symptoms related to low thyroid in the brain (for example) but

the thyroid doesn't do anything about it. But if you give thyroid

hormones in an adequate dose the brain symptoms will disappear.

Meanwhile the other tissues and organs adapt to the increased

circulating hormones that you have used to fix the brain with. The

adaptation of the tissues to different levels of circulating

hormones has been shown in the literature.

The symptoms of low thyroid, which are numerous and variably

expressed, can be related to any organ or system in the body and

partly depends on the person's genes. But because of the all

inclusiveness of the TSH medical students are not taught or only

superficially taught the symptoms of low thyroid. The TSH

was " scientific " and held all the answers to thyroid disease. If you

have not lived through several versions of the ultimate test for

thyroid then it is harder to grasp this phenomenon.

Shomon: If, as Dr. Weetman suggests, the laboratory's reference

range for " normal " TSH includes people who are in the process of

developing hypothyroidism, do you feel that the reference range

itself should be recalculated?

Derry: This suggestion agrees with what I have been saying

namely that the TSH can lag a long way behind the appearance of low

thyroid symptoms. One clear case I remember is a lady who started to

lose her hair at age 26 and had lost it all by the time she was 35

but the TSH did not turn up until she was 48. Then her TSH rose very

high for the first time. (The TSH was several hundred). She was

being treated for a heart condition at the time but when the

cardiologist saw the TSH, he said just treat the low thyroid

condition and her heart problems will go away. He was right. Her

hair has not grown back yet. She has been taking thyroid for about 1

year now. So her TSH lagged her symptoms and signs by 22 years. In

some cases the TSH appears never to turn up and confirm the clinical

diagnosis.

It is difficult to visualize using the TSH when, as Dr. Weetman has

said, people can be low thyroid with a normal TSH. The truth is that

there is no relationship between the TSH and how people feel. Dr.

Toft has stated this in the bible of thyroidology Werner and

Ingbar's " TheThyroid " in 1991. I have quoted this reference in my

response. Dr Weetman has also said in a response on line to the BMJ

article of May 2000 article by Denis StJ. O'Reilly on " Thyroid

function tests_time for a reassessment " that he thinks that a

patient can have a profound hypothyroidism without any signs or

symptoms. This is incorrect.

To follow the TSH while you are treating someone for low thyroid is

also going to lead to under-treating the patient. The pituitary

cells, which have TSH in them, are the most sensitive cells in the

body circulating thyroid hormone. Therefore when one treats

hypothyroidism by following the TSH and trying to make it normal the

pituitary cells are happy but the rest of the body is short-changed

by a considerable amount I also mentioned in my response to the same

article that the normal dose arrived at by all the best clinicians

in the world over 80 years of experience was between 200 and 400

micrograms of Eltroxine. But some need more. Currently treated

patients average about 100 micrograms which is about a third of the

dose that has been known for a century to help patients return to

normal. Long term studies found no difference in any disease between

normal people and people taking the thyroid at the higher doses.

Recent studies have confirmed this opinion. The tail end of this

approach of the method of treating hypothyroidism was documented by

Professor R. Hoffenberg in the introduction to his two part article

on hyperthyroidism in the British Medical Journal 1974. Reflecting

on a life-time of treating thyroid patients, he mentions that his

personal record of amount of thyroid he needed to give to a patient

to make them feel right was 29 grains of desiccated thyroid. which

represents approximately 1700 mgs of desiccated thyroid which would

be equal to about 2900 micrograms of Eltroxine. This highly-

respected thyroidologist had spent a lifetime treating thyroid

patients must have prepared the paper and had it accepted during

1973 when the consensus meeting on the TSH occurred.

This all means even if the chronic fatigue patient does have an

abnormal TSH the treatment will be inadequate to make them well

again. The clinicians of the past (before the TSH) were astute and

very observant and were able to diagnose and treat hypothyroidism

correctly without the TSH for 80 years-- why do we need it now? They

would be aghast at the total missing of the diagnosis of chronic

fatigue and fibromyalgia.

The treatment of thyroid cancer before the TSH involved giving the

maximally tolerated dose of thyroid in order to stop the cancer. It

was termed then a sub-toxic dose. That is the dose of thyroid would

be raised until some toxic symptoms occurred then the dose would be

lowered slightly to remove the symptoms such as sweating too much or

tachycardia. The present treatment of thyroid cancer patients only

get enough to suppress the TSH which is usually a much lower amount.

Nothing untoward happened to these patients of the era before the

TSH because of this higher thyroid dose.

Shomon: You indicated that you feel chronic fatigue and

fibromyalgia are both hypothyroid conditions. There are some

physicians who feel that these two conditions are manifestation of

difficult to diagnose hypothyroidism, and yet other studies claim

there is no relationship. Can you explain why you feel there is a

connection among these conditions?

Derry: For many years the literature (before the TSH)

supported the fact that if your symptoms responded to thyroid

hormone you were low thyroid but especially if when you took the

person off the thyroid and their symptoms returned. My own patients

who develop chronic fatigue or fibromyalgia I treat them with

thyroid and all --and I mean all-- of their symptoms disappear. If I

stop the thyroid or if they stop it for some reason all the symptoms

start to slowly come back over the following months. You might ask

do I do thyroid function tests? The answer is yes if for no other

reason that I am curious to know what they look like in the face of

the patient's obvious clinical diagnosis. The other patients who

come to me from outside my practice respond roughly in proportion to

how long they have had it. But I have had lots of pleasant surprises

of people badly disabled by fibromyalgia or chronic fatigue for six

years or more who slowly over 6 months to a year their symptoms

completely disappear. It is of course a delight to see this happen.

Shomon: Do you feel that TSH - or TRH, T4/T3, antibodies, or

Reverse T3 - tests have any place in thyroid diagnosis and

management, or do you believe that diagnosis and treatment should be

solely based on symptoms.

Derry: One place that TSH has been useful is testing new-born

babies. The TSH which is backed up by the free T4 or the Total T4

tells you quickly that the baby has a serious problem which must be

treated immediately. This does not say that the TSH is infallible in

this instance but at least when it is abnormal then you know you

have a serious problem.

A phenomenal number of thyroid function tests are ordered by

physicians today but it is unlikely that it has helped that much as

the physicians have been ignoring the symptoms of low thyroid which

so many patients complain about.

[Guest guest]

Janie, Makes sense, but again my experience with small doses of Cytomel

for 3 days produced what I assumed were symptoms (ie. Skeletal muscle

weakness-you know that weird, awful feeling in your muscles that only

thyroid patients seem to understand and Endos never do) as a result of

the quick rise in T3 levels??? That episode remains a mystery to me,

and leaves me somewhat apprehensive of taking a product, Armour, that

contains so much more T3. In all fairness I recall that for the last 2

weeks of my 6 week " prep " for my 2 scans I took larger doses than 5 mcg.

for the prep without that happening???

In regards to the Docs not understanding the awful feelings that we

thyroid patients feel, wouldn't it be great if we could get them to

take say 100mcg of their favorite T4 product for 6 months and " walk the

walk " for a while. I don't sound angry, do I?

Re: TSH

>but I thought I read a " medical " explanation for that as opposed to

>a " I just feel better " explanation.

The TSH is the message sent by the pituitary gland to the thyroid to

do it's stuff. (It stands for Thyroid Stimulating Hormone.) The

pituitary gland is simply a messenger. If it senses that there is

enough thyroid hormones in the body meeting the needs of the body,

it doesn't have to send much of a message, via the TSH, to the

thyroid to produce, because the thyroid has already done it's job.

The pituitary gland has NO idea if the thyroid is sick or not. It

just sends a message.

In the hypo person, or a person with a " diseased or sluggish

thyroid " , the ideal state is to put enough hormones in the body, via

Armour, so that the pituitary gland hardly feels the need to send a

message to the diseased thyroid. The ARMOUR is taking the place of

the thyroid.

And if you are not putting enough Armour in the body, the pituitary

gland is going to send a message to the thyroid, via the TSH, to

make up the rest. BUT the thryoid CAN'T make up the rest!!!!!!! So,

for example, if you are only introducing enough Armour to make your

TSH at 1.5, for example, the thyroid, via the TSH, CANNOT make up

the difference that you might need due to a particular activity or

need!!!!

So, docs have found that the only way to OPTIMALLY support the body

with Armour is to give it ENOUGH to suppress the TSH, which also

ends up being a free T3 in the upper part of the range, if not

slightly over.

Make sense??

Janie