tilbake til binyresiden

slitne binyrer pga. hypothyreose

Det fins autoimmun binyrebarksvikt, og det fins det tester, hovedsakelig anti-21-OH hydroxylase

Men i forumene utenlands og innenlands støter en alltid på en del personer som tar eller vil ta noe
hydrocortison for "weak adrenals" som er en mere eller mindre forbigående form knyttet til
hypothyreose. Grunnen er at binyrenem må jobbe hardere, altså det er stress på binyrene når en
er hypothyroid over tid.

Se Durrant-peatfields gamle artikkel om emnet

Mange kan da etter en stund slutte med cortison og bare ta sin dose med Levaxin eller Armour.

Det er ikke mye skrevet av leger, Addison er mere anerkjent.
Dr. William Jefferies har skrevet en hel bok om dette, Safe Uses of cortisol, kan bestilles fra forlaget.
Dr. Durrant Peatfield "The Great Thyroid Scandall and How to Survive It -kan finnes på thyroiduk.com sin webside


Her er noen uttalelser fra newsgroups of internettforumene:

>To S: It sounds like you take Cortef on a continuous basis.
>I thought it was meant to be taken only for a few weeks, to give the
>adrenals a rest and restore the balance in the system.

The doctors who are actually good at treating chronic fatigue are willing to
give Cortef on a long term basis. That said, it depends on the individual how
long they will need it. In the UK, Dr. Durrant Peatfield (his new book "The
Great Thyroid Scandall and How to Survive It" gives and excellent explanation
of concurrent adrenal / thyroid treatment) found that in some cases, if Cortef
was started the patient got better and wouldn't need thyroid hormone and
sometimes the Cortef was only needed temporarily.

I don't have Addison's Disease, only mild adrenal insufficiency. Those with
more severe adrenal problems find they collapse if they skip their dose, or
even don't gradually taper it down if they were taking more than their normal
amount. On the other hand, I gradually worsen over a period of a few weeks to
a few months if I forget it. No collapse. Only a gradual increase in the
feeling of not being well.

When I went on Cortef, I felt much better the first day. Within a short time
my chest pain (costochondritis) went away, "rheumatoid" the doctor said I had
in my hips went away, digestive pressure and constant bloating of the stomach
went away and so did a problem with annoyingly frequent urination. The stuff
really helped me. Whereas I can't tell I need it now on a daily basis, I can
tell when I go off a while and it's easy to forget when you can't tell it makes
a difference.

Anyways, as long as your at replacement doses (5 mg 4 times daily which equals
20 mg per day and is equivalent to about 5 mg of prednisone) as opposed to the
huge doses of the emergency room equivalent, prednisone, there are no long
term side effects, you're simply supplementing a natural hormone that has a
tendency to run low. Doctors do shy away from giving Cortef, yet they would
give my wife 60to 80 mg of prednisone without trying lower doses when she came
to the emergency room. (Before thyroid treatment she had severe allergies and
asthma and it seemed her throat would swell up just from breathing. The
allergist knew she had a thyroid problem, it was too severe to be simply
allergies but after running all the labs he knew, he couldn't confirm it. She
finally got better because a doctor treated her symptoms and not her lab

William Jeffries, author of "Safe Uses of Cortisol" claimed that on Cortef,
your adrenal reserve is higher, that is the cortisol you have available for
emergencies when you need it will actually be there. I believe it.

Jeffries also said that many people who had normal lab tests but were
symptomatic would improve on Cortef. The labs aren't that great for diagnosis.

I read an article on a medical school website with interest once. It was
summarizing an endocrinology journal and telling how a patient came in with an
adrenal crises. (You die when this happens, I think of circulatory breakdown.)
He also had Hasmimoto's with high antibody levels historically. (Antibodies
can also attack the adrenals, but are rarely tested for.) Anyway, they treated
him with corticosteroids for a period of time. When the treatment was
complete, he didn't need adrenal sumpplementation and he no longer had Hashi's

Anyway, my suspicion is if one goes on Cortef, they know if they can stop it
completely after a while or if they really need it, and if they want they can
experiment and see if their adrenals are rested, or like their thyroid needs to
be supplemented for life. I prefer supplementation over my chest pain being so
bad at times I wonder if I'm having a heart attack. (Per the Mayo Clinic
website, costochondritis can be that bad for some, it was for me.)

Here's an excerpt from Dr. Barry Durrant-Peatfield that used to be online, and
is also covered in his book.

5. Adrenal Insufficiency

This might be more properly described as low adrenal reserve. Since
hypothyroidism adversely affects every cell, every tissue, and every gland in
the body it is clear that the endocrine system as a whole will be also
similarly affected. The adrenals will be subject firstly to lowered efficiency
resulting from a lowered vitality primary to hypothyroidism, and secondarily,
to reduced ACTH stimulation from the pituitary. As a result, in general,
patients with a protracted and/or severe hypothyroid state will have some
degree of adrenal insufficiency. A significant level of this will be suspected
in these situations:

a. Longstanding and severe hypothyroidism.
b. Episodes of extreme exhaustion, or collapse.
c. Bad response to minor illness.
d. Multiple allergies.
e. Digestive problems – alternate diarrhea and constipation
f. Flatulence
g. Weight loss
h. Increasing arthralgia (fibromyalgia) and morning stiffness.
i. Pallor, yellow pigmentation (due to poorly metabolized carotene)
j. Fainting, dizziness

These patients often present with dark rings under their eyes, looking quite
ill. Blood pressure is low, with a positive Raglan’s sign. (Pressure fails to
rise on standing). These symptoms and signs, it will be appreciated, are those
of the early phases of Addison’s Disease.

A single estimation of blood Cortisol is usually unhelpful, but
De-hydroepiandrosterone sulphate (DHEA), the main hormone output from the
adrenals, will be found to be low. Depressed levels in the endocrine system as
a whole are likely to be found. The low adrenal reserve means patients are more
or less well, until challenged by the stress of illness or life events--even
the thyroid replacement therapy itself initially. And this partial failure will
affect adversely T4-T3 conversion and the integrity of the thyroid receptors.

It is essential to manage this insufficiency where present, or where suspected.
Remarkably, patients with symptoms, signs and blood pathology of low thyroid,
may improve completely on management and correction of the adrenal problems
alone; as conversion and receptor efficiency improves, the thyroid hormone
circulating - partly unused - is brought into play.

Adrenal insufficiency is dealt with by the provision of the two hormones most
likely to be lacking; Cortisonehydrocortisone, and DHEA. (as pointed out above,
low DHEA may be used to infer low cortisone output). The treatment therefore,
is the exhibition of, ideally, Hydrocortisone. This should be given in divided
doses initially of 5mg qds; after a week, 10 mg qds may be used. This remains a
physiological dose, not challenging or suppressing the adrenal function, but
supplementing it. In these doses all of the usual anxieties associated with

cortisone do not apply, since restoration of normality is being aimed at.

This may need to be explained to patients long subject to media-induced fears
of the horrors of corticosteroids (Their physicians may share these anxieties,
unnecessarily). Dr McCormack Jeffries’ papers on the subject are most worthy
of study. DHEA has reached prominence in recent times as a hormone of multiple,
and magic properties. Certain it is that the adrenals secrete more DHEA than
anything else, and the amount is inversely proportional to age. It is
metabolized to oestrogen and/or testosterone, but also has been shown to play a
role in reducing obesity; in reducing atherosclerosis and cholesterol; it
inhibits the glucose -6-dehydrogenase enzyme in cancer; it improves immune
response, and, possibly, acts as a neural facilitator. In physiological doses,
there seems to be no problem in its long-term use. If levels are demonstrably
low, it is reasonable to provide replacement therapy.
You know, I've only found this Ligament Stretch Syndrome in relationship to low

You've said you had "high adrenals." I'm not quite sure what you meant by
that. My wife has high adrenals, her AM cortisol always comes back well up in
the range and if she ingests caffeine or sugar I believe what happens is her
catecholamines (adrenaline, norepinephrine) start producing and she has tons of
energy. Not short-lived either. I never understood it, I would drink 2 liters
of Mountain Dew hoping for a little energy. She would drink a little cup of
coke and not be able to contain herself.

Anyway, the adrenal doctors say that if your cortisol levels are high, that can
be a beginning stage of adrenal fatigue and may even last for years that way.

So, if this Syndrome really only applies to low adrenals (I suspect anythng
that can apply to low adrenals can apply to low thyroid, but who knows), then
perhaps that's part of the reason for your fatigue and brain fog?

I know I've read somewhere that hypermobility is common in low thyroid. I know
I can easily put my hands flat on the floor, which I used to think was a good
thing. I don't have any of the other typical signs for hypermobility though.
I don't know about you, but I was hypo from a very young age. My brother used
to ask my mother why I slept so much. At 3 or 4 years old she took her first
picture of me sleeping somewhere. It was cute at that age in a rifleman shirt,
wasn't quite so cute laying half on and half off the couch at age 18, in spite
of what she thought.

> I think that what they
>term as ligament stretch is associated with adrenals but the fact is that
>there are those of us who have hypermobility syndrome - the same thing -
>that has nothing to do with adrenals.

Below is from Dr. Rind's chart comparing the symptoms of low thyroid to low
adrenals. He thinks the ligamernts as well as the hypermobility are more
related to adrenals.

I think it's too difficult to categorize between the two. My wife has high
cortisol levels, from reading the chart I would think she was hypoadrenal, I
think she has more adrenal symptoms than I do, but she has high adrenals with
low thyroid.

Signifies low adrenals -
Lax ligaments or flexible (e.g. flat feet, double jointed). Joint
strains/sprains are common.

Signifies low thyroid -
Poor flexibility.

Low Adrenals


by Dr Barry J Durrant-Peatfield

M.B., B.S., L.R.C.P., M.R.C.S.

86 Foxley Lane Purley
Telephone - 020 8660 0905

Cortisone therapy was first brought to the world of medicine in the thirties, by
the work of Hench & Kendal. By the late forties, and early fifties, cortisone
was hailed as a medical breakthrough in the treatment of rheumatoid arthritis,
and similar illnesses, asthma, and as a lifesaver in the management of surgical
shock. Yet, within a few years, doctors and patients alike, became fearful of
its use; an anxiety which persists very much today, thus denying many people
enormous benefits.
The problem lay in dosage. Really quite large doses were given - and sometimes
are today - which caused various side effects. The swelling and puffiness of the
weight gain, osteoporosis, peptic ulceration, bruising, fluid retention are
generally quite well known. Yet these occur only in doses way above the natural
levels of cortisone in the body; what we may call "pharmacological" doses. This
collection of symptoms - or syndrome - occurs in nature when the adrenals become
seriously overactive; this is called Cushings Syndrome.
What was not realised until quite a lot later, and regrettably in some quarters
still today, is that cortisone in small amounts, used as replacement therapy,
for deficiency, can be of extraordinary benefit, and cause no side effects of
any kind. This is the use of cortisone replacement therapy in physiological
doses, when the side effect problem no longer applies. The use of a cortisone
derivative in your treatment is in this way; to correct a deficiency, brought
about by low adrenal function.
The adrenals sit just above the kidneys in the loin, one on each side. Their
tasks are many and varied; and are so important, that if you lose your adrenals,
you die within three days. The inside of each adrenal produces adrenalin, which
is the hormone that gives us a sudden burst of energy or strength when
confronted with a crisis situation - the "fight or flight" scenario. It is the
rim, or cortex, of each adrenal, that most concerns us for the present. It
produces a number of complex hormones with vital roles to play, and are
essential in the system's response to prolonged stress; e.g. infection, injury,
starvation, massive exertion. The first group is the glucocorticoids (mostly
hydrocortisone), whose job is mostly to stimulate conversion of protein to
glucose; and maintain the tone of the vascular (or blood vessels) system.
The second group comprises the mineral corticoids, which regulate the proper
balance in the body of sodium and potassium, and are therefore to do with fluid
retention and blood pressure. Aldosterone is the chief. The third type are the
androgens, (male sex hormones), and are represented by Dehydroepiandrosterone,
(DHEA for short), and androstendione. These have as their main job, the
promotion of repair and growth in the tissues.
Fourthly, are the oestrogen's, that back up the oestrogen made by the ovaries -
as, for example, in the menopause. Other hormones are suspected, but not yet
isolated. The output of these hormones is cyclical, with maximum level early in
the morning, and least at night.
Our deepest concern here, is the crucial importance of the adrenal cortex
hormones in the system's response to stress. Briefly, there is a rapid increase
of the glucocorticoids, to enable the body to cope. It is the failure of this
mechanism to work properly, in the presence of general stress, or the stress of
illness, that we are concerned with in the use of replacement cortisone therapy.
This condition we call Low Adrenal Reserve, or simply, Adrenal Insufficiency.
The most severe form of the syndrome is called "Addisons Disease", after the
great Guys Physician, Thomas Addison, who was the first to describe it in 1855.
It was then usually due to tuberculosis destroying the glands. Patients were
dusky coloured, with terrible weakness, malnutrition, collapse and coldness, and
the illness ran a fatal course. It is pretty rarely seen in clinical practice.
But we are concerned with the mild form of deficiency, where the patient may be
well, until subjected to stress and/or illness. Then, many of the symptoms may
appear with prostration and collapse; or there may be a level of insufficiency
present all the time, with varying degrees of weakness, muscle and joint pains,
and general ill health.
So what do we look for in the way of symptoms? It is rarely clear cut, because
the deficiency is so often part of another illness, and may therefore have
something of the symptoms of both. We are particularly concerned with thyroid
deficiency, which, if of longstanding, or fairly severe in degree, is most often
associated with adrenal insufficiency, as well as a direct result of the stress
on the system low thyroid function will cause.
The patient will complain of weakness and episodes of prostration, frequently
feeling quite unwell without being able to pinpoint the cause. Episodes of
dizziness, sometimes cold sweats, caused by the blood sugar becoming abnormally
low, are not uncommon. Often, an odd internal shivering is described. Aches and
pains of a rheumatic nature are other frequent complaints. The patient often
complains of the cold, and is likely to be cold to the touch. The subject does
not feel well, and may look ill, with dark rings under the eyes, and a general
pallor. There are likely to be digestive problems, with excessive wind and
bloating, and bowel disturbances. The menstrual cycle may be disturbed, or
absent; libidos low. Depression and anxiety may also be a feature. Some of the
symptoms complained of by patients with M.E. - Myalgic Encephalitis - are very
similar, leading to the well grounded suspicion that M.E. is associated with low
adrenal reserve. Certainly, frequent minor illnesses are common, with an
overlong course of quite minor infections, which may also have an unusually
severe effect on the patient.
Low thyroid function has some of these features, and it may be difficult to
distinguish one from the other; In fact it should not be necessary because, as I
pointed out above, as the two are often together, so too must the treatment
overlap and be designed to relieve both.
The complications of treating hypothyroid or under active thyroid patients) is
that their consequent poor adrenal reserve may become suddenly obvious, as soon
as the thyroid is treated. The thyroid supplementation may, at worst,
precipitate the adrenal problem; but what usually happens, is that the thyroid
replacement may either not apparently work at all, or the patient may have
thyroid overdosage symptoms on quite a low level of replacement. Hence, where
low adrenal reserve is suspected, it is possibly dangerous, and certainly ill
advised, to treat the patient without supplementation of the adrenals, in the
manner explained further below.
If a high index of suspicion of adrenal insufficiency is raised by the history
given by the patient, then what are the signs the doctor looks for to establish
the diagnosis? Actually, it is sometimes difficult where the problem is not
particularly severe; but there are some pointers. The blood pressure is usually
quite low, often very strikingly so. The difference between the lying, (or
sitting) blood pressure, and the standing one, may be very important. Normally,
it rises when the patient stands. In low adrenal reserve, it either does not
change at all, or lowers further. The pupil reflex is slow, or unstable, or even
reversed, to bright light. Reflexes may be abnormal, especially the Achilles
reflex - in the heel. The heart sound is characteristically altered.
It is satisfactory to confirm the clinical impression by blood tests; but these
sometimes are unhelpful. The level of cortisone in the blood may be measured,
but it is widely variable. However, DHEA, mentioned above, is quite a good
indicator of adrenal cortex function. The urinary excretion of adrenal hormones
is an excellent indicator - but the practical problems, (it has to be over 24
hours), and the expense of really good laboratory analysis, tend to limit this
test to hospital inpatients. It is, in our view, perfectly practical and
reasonable, to establish the diagnosis on clinical grounds, and because the
therapy given is of very low - physiological - doses, there is no possible risk
to the patient, however long it is needed. In a very large number of cases, the
adrenal insufficiency may right itself over two or three months, making further
supplementation unnecessary.

The Treatment
You will be given hydrocortisone lO mgm, which is the natural form, to take in a
dose appropriate to your needs. Half a tablet three or four times a day is
usual, later to be increased, if required. Hydrocortisone has the problem of
very rapid uptake by the system, and it needs to be given every four hours, at
least. This creates practical problems for many patients, and we use more often,
Deltacortril, or Prednisolone. 2.5mgm is usually given to start with, increasing
to 5mgm after a few days. Rarely, a total dose of 7.5mgm may be required.
Most patients feel benefit within a few days. You will be asked to ring the
surgery if you are in the slightest doubt about how you feel, or how things are
going. Are port by phone after a week is pretty important, and then we see you
in two or three further weeks to assess matters. You will probably have been
asked to keep a diary of events. If you have a thyroid problem, the thyroid
replacement will start after a week, at a very low dose, working slowly upwards.
It sometimes takes many weeks for all the benefits to come through, but some
improvement is clear within a week or so. Adrenal insufficiency related to low
thyroid function corrects itself, as the thyroid levels improve, and usually
after, two, three or four months, have recovered sufficiently for the cortisone
therapy to be stopped.
The question is often asked. Will the cortisone replacement suppress my
adrenals? The answer is that in physiological doses it does not at all; and in
any event, the adrenal activity is curtailed anyway, making the options quite
clear. Suppression occurs in the superpharmalogical doses, which do not concern
us in this context. Even then, the adrenals are able to recover if the primary
illness is dealt with, and the dose reduced gradually.
Low adrenal reserve means that under a state of challenge, the problem is going
to show. While on replacement treatment therefore, any further illness and
stress is best dealt with by a temporary increase of dose. Influenza, heavy
colds, dental extraction, injury and the like, require, for example, the 5 mgm
Deltacortril to be doubled, just for a few days. (I find that a 5mgm dose almost
completely prevents jet lag; and influenza is over in one or two days.)
We have now a considerable fund of practical experience in the treatment of the
adrenal deficiency syndrome, and are very much aware of its great benefit.
It should not be considered in isolation, however, any may well be part of the
management of other deficiencies. The ageing process is the result of deficiency
in a number of different aspects of the system; so that full benefit may not be
gained until both nutritional and hormonal imbalances are looked for and
During the time we are assessing your medical problem, we will include all that
I have been talking about, as well as those aspects related to the menopausal
situation, both for men and women.

[ Home ] [ HYPOTHYROIDISM ] [Low Adrenals]


by Dr Barry J Durrant-Peat field
M.B., B.S., L.R.C.P., M.R.C.S.

Approved Civil Aviation Medical Examiner

The clinical syndrome of thyroid deficiency is very much more common than is
generally realised; Barnes, in several publications, drew attention to this in
the last two decades, as has the present writer more recently. One reason for
this, is a tendency to think of hypothyroidism and rnyxoedema as one of the same
thing, when this is quite wrong. Myxoedema, as doctors were taught in medical
school, is the end result of a progressive disease process resulting in more or
less total absence of thyroid hormone; whose symptoms and signs are no doubt
perfectly familiar. But this state of deficiency has to start somewhere, winding
down over a variable period to the terminal state of myxoedema. Symptoms and
signs will naturally vary according to the extent of the level of deficiency
reached. Clearly, a 10% loss may have little to show for it; whereas a 25% loss
may have several very definite symptoms and signs; and a 40% loss even more so.
Furthermore, patients show very individual response to any given level of
dysfunction; while one may complain of excessive fatigue and weight gain,
another may be more troubled by depression and menstrual problems.
That the diagnosis is all too frequently missed, is an inevitable result of
this fundamental misunderstanding, and is commonly the result of an incomplete
clinical appraisal in favour of the standard thyroid function tests. These tests
are the real problem in diagnostic failure since there are inherent problems in
interpreting blood levels of thyroxine and/or thyroid stimulating hormone (TSH)
when blood levels may differ widely from tissue blood levels. Since the
diagnosis may very properly, and easily, be made clinically, unreliable blood
levels should NOT take precedence over clinical judgment.
Equally unsatisfactory is the acceptance by doctors and patients alike of
poor response to thyroid replacement.
The present writer has been constantly alarmed and dismayed by hypothyroid
patients who for years, all too often, have been obliged to accept a much less
than satisfactory amelioration of their illness, being taught to expect no more
than some improvement. It is perfectly possible that complete and long lasting
remission should be obtained, and neither doctor nor patient should accept
anything less. Further, the response should be monitored, not just by the
doctor, but by the patients themselves. Since there often is a dynamic
situation, the patients should be educated and taught to monitor themselves,
making their own adjustments to dosage. In this connection, frequent monitoring
by blood tests may be quite misleading and unhelpful. Surely it must be more
satisfactory for the physician to ask the patients how they feel; and guide the
informed patient in establishing the right dosage levels of replacement therapy.
One of the most taxing problems in diagnosis is the multiplicity of
symptoms, which need not be rehearsed here. It is all too easy to pigeonhole the
polysymptomatic patient as one of the heart sink variety, and much too often,
for example, inappropriately exhibit, perhaps, Prozac. Thyroid deficiency may
cause all sorts of major and minor symptoms; and their very frequency should
raise an index of suspicion for thyroid deficiency. The simple Basal Temperature
Test, (see below), wrongly derided by many authorities, can provide valuable
clinical backup. Finally, there is nothing wrong with a thought-fully planned
trial of treatment with an informed and co-operative patient.
Hypothyroidism is due either to:-
A. Deficiency of thyroid hormone production;
B. Failure of thyroid hormone to reach the tissues.

Both may operate together in varying degrees.
Deficiency of hormone production is due to:-

1. Environmental Toxins/ deficiencies
2. Genetic thyroid failure
3. Thyroid failure secondary to pituitary insufficiency
4. Thyroid surgery
5. Treatment of previous overactivity
6. Major surgery
7. Tonsillectomy
8. Major trauma
9. Glandular fever
Failure of hormone to reach the tissues results from:-

1. Receptor resistance, or failure
2. Dysfunction of T4T3 conversion
3. Adrenal insufficiency
Dealing in turn with the therapeutic management of these problems, we may turn
first to (A) Thyroid hormone production failure. This will be due to:-

1. Environmental toxins and deficiency

(A) Toxins
A number of chemical agents tend to interfere with the manufacture of thyroid
hormone. Notables among these are:
Poly chlorinated Biphenyls (Paints and wood preservatives)
Resorcinol (Millet)
Phthylate Esters (Plastics)
Thiouracil (Cabbages, Turnips, Cassava.)
Cyanides (Barbiturates)
Thiocyanates (Smoking)
The elimination of these from the diet may be desirable, if not always

(B) Nutritional Deficiencies
(i) Iodine. Endemically absent in certain inland areas e.g. (Peak District)
(ii) Minerals in particular: Selenium
(iii) Vitamins.

Vit A - Conversion of Carotene to Vit A is inhibited by low thyroid states, and
may cause yellow pigmentation.
It controls uptake of Iodine into the thyroid gland.
Deficiency also reduces T.S.H
Vit B Riboflavin, Niacin, Pyridoxine play a role in thyroid hormone manufacture.

Vit C & Vit E

Deficiency has been shown to cause hyperplasia at cellular level in the thyroid.
Clearly, part of the management of hypothyroidism requires some dietary
advice; the provision of iron and vitamins and other minerals is simple and
2. Genetic Thyroid Failure.
This will have become apparent soon after birth; but may not be obvious
cretinism. A sickly child, with poor weight gain, frequent infections, lethargy,
or oddly enough, hyper kinesia, and is a candidate for genetic poor thyroid
function. Thyroid replacement is mandatory as early as possible.
3. Pituitary Failure.
This is a more common problem than is recognised, and apart from its
specific clinical features, it may be a cause of secondary hypothyroidism. The
pituitary may have a genetic deficiency, when it will have been probably
recognised early. Not uncommon is Sheehan’s Syndrome, resulting from major
trauma from accidents or surgery. Adenomas of the pituitary may cause pressure
atrophy and / or abnormal hormone outputs. But the pituitary may be involved in
the general multiple deficiency state, and more specifically in low thyroid
states. This partial failure in hypothyroidism may well be a cause of low T.S.H,
so that a vicious spiral may slip into being. The danger of a low or normal
T.S.H in this situation being mis-interpreted when thyroid function tests are
carried out is quite clear. In this situation, correction of the thyroid state
will bring benefits to the pituitary; and may explain why some patients on
thyroid replacement therapy begin to need lesser doses as time passes.
Correction of the thyroid deficiency is clearly necessary; but adrenal
insufficiency, considered in more detail later, as a consequence of lowered ACTH
output, may require cortisone and Dehydroepiandrosterone (DHEA) in addition.
4. Thyroid Surgery.
This is undertaken as a treatment for pathology of the thyroid itself, or as
a treatment for overactivity, discussed below. Thyroid cysts, Adenomas or
Carcinomas are necessarily removed by surgery; and it is sometimes necessary to
remove goitres where the size is causing respiratory or oesophageal
embarrassment. Hashimoto’s disease may come into this category.
Replacement by thyroid hormone is an obvious consequence.
5. Treatment of previous thyroid overactivity, by surgery or 1131 ablation.
Grave’s disease is widely treated, where medical methods are deemed
unsatisfactory, by partial thyroidectomy, or Radioactive Iodine ablation. This
is often unsatisfactory, since it is very difficult to get it right. Either too
much is removed or destroyed; (in which case replacement therapy is a permanent
necessity) or too little, and it may have to be done again.
For such patient's replacement therapy is an obvious no option requirement.
6. Major Surgery,
Most particularly in this context comes cholecystectomy and hysterectomy.
Many doctors are aware that women may suffer weight gain and loss of well being
after this surgery; and this will be found to be due to early loss of thyroid
function. Replacement therapy is required.
7. Tonsillectomy.
Quite why in adults tonsillectomy may result in slow running down of thyroid
function, is not clear, but may be the result of interruption of the blood
supply. The present writer has noted a number of cases of young adults
misdiagnosed as M.E sufferers in this situation. Replacement therapy provides a
most satisfactory return to normal.
8. Major Trauma,
Major road traffic accidents, and surgical accidents are known to
precipitate thyroid and/ or pituitary insufficiency. In this category have been
noted the major psychic trauma of certain life events. Replacement indicated,
with regard given to pituitary - adrenal function.
9. Glandular Fever.
This is an often met with cause of failure of the thyroid/ adrenal axis.
Evidence has pointed to pituitary damage causing secondary hypothyroidism; But
progressive loss of thyroid producing cells within the thyroid has been noted.
In either event, replacement is required. Discussion of failure of uptake at
tissue level may be conveniently dealt with in the section below on therapeutic
options. Consideration should now be given to the aims of replacement therapy.
The overall purpose is to restore metabolism to normal, so as to eliminate
all hypothyroid symptoms, and to secure a sense of normal well being. This
implies that thyroid hormone levels in each and every cell are nominal; that all
the exchange reactions are taking place, as they should be. Sadly, this ideal is
at least as often as not, simply not reached, often by a long way. Residual
tiredness, lack of drive, depression is frequently admitted to. Menstrual
dysfunction may remain a feature. Skin problems, fluid retention, digestive
problems, arthralgia, may remain in some degree. Many patients will continue to
com-plain of weight gain, or great difficulty in losing it, and receive scant
In this situation, the physician may estimate thyroid function by Free
Thyroxine Index (FTI), or Thyroid Stimulating Hormone (TSH); and be confronted
by normal readings. It is the present writer's view that these estimations may
be seriously flawed, and their value fundamentally limited. The most popular, at
the moment, is the TSH. This may be much affected by poor pituitary function
itself due to hypothyroidism; it may be low or normal, rather than raised. The
FTI is subject to several errors. Poor tissue uptake is probably the most
telling. If the actual use by the tissues is reduced by poor conversion of T4 to
T3 (see below) and/or receptor block, then high or normal blood tests will
result. Haemoconcentration may be an additional factor.
There can be no substitute for proper clinical appraisal. If the patient
sounds and looks hypothyroid, then probably that is the problem - irrespective
of pathological testing.
The net result very much too often in clinical practice is to underdose. To
provide full remission of symptoms, the level in the tissues of thyroid hormone
should be as high as possible, short of too much. (The patient/doctor monitoring
to achieve this is described later). The situation is worsened by a tightly held
misapprehension in many quarters that there are grave risks associated with
overdose. These are largely apocryphal and must be corrected. Probably most
widely held, is that thyroid overdose is bad for the heart. The risk is there if
coronary artery insufficiency, previous M.I or incipient failure already
compromises the heart; the risk of over working a damaged heart is obviously
undesirable. The healthy heart will not be damaged by minor degrees of overdose,
whether by accident or design; and is rarely much affected even by high levels
of thyroid hormone, as in Grave’s Disease.
Another anxiety is osteoporosis. There is a risk in sustained overdose, and
untreated hypothyroidism, but this is still not certain. There is NO risk of
osteoporosis in thyroid supplementation in correct, physiological doses
obviously; and in any inadvertent minor overdose is rapidly detected by
monitoring, and therefore of no consequence either.
Suppression of the thyroid gland as a result of treatment is another
frequently expressed anxiety. There is a sensitive negative feedback operating
through the hypothalamus and the pituitary Overdose will suppress the thyroid;
but this will come back to normal at once when the dose is adjusted. Not
treating a patient with an under active thyroid for fear of promoting further
depression is quite unrealistic.
Vague fears that thyroid is like "speed"; that any deliberate or accidental
overrunning of the metabolism will result in early "burn out"; have been
expressed. All that can be said is that is simply not true.
The correct management of thyroid replacement requires a flexible approach;
full explanation to the patient, and monitoring, relying as much on the patients
assessment as the physicians own clinical impression. One may often be obliged
to deal with partial response to replacement therapy, with failure to respond to
an increase of dose; and more wrongly, some symptoms of overdose on small levels
of treatment. These will include raised pulse rate, tremor, breathlessness,
headaches. Sometimes an encouraging response levels off and drops back.
To understand what is happening, it should be clear that five matters have
to be considered in planning replacement therapy:
1. Dose
2. Vehicle
3. Conversion T4 - T3
4. Receptor resistance or deficiency
5. Adrenal insufficiency

1. Dose. This has to be infinitely variable. It starts low and will be increased progressively and incrementally, until full response is obtained.
Neither doctor nor patient should be satisfied with 60% response; or 80%; 100% is the target. The patient will be asked to monitor their response to treatment.
This is satisfactorily done by three simple exercises.
1. Basal Temperature, this is the temperature (10 ins Axillary, or 3 ins in
mouth) immediately on waking. It is low in hypo metabolic states, but will rise,
albeit slowly, in response to treatment, (as reported elsewhere this is valuable diagnostically). A sudden rise may indicate, all things being equal, the start of overdose.
2. Basal Pulse. This may be taken at the same time as temperature; overdose will result in a rise of the resting pulse. 80 bpm will usually signify overdose.
3. "Feel good factor". It is possible to ask the patients to make a
subjective assessment, say, one out of ten, on the same days as temperature or
pulse. Since improvement in thyroid replacement may be quite slow, placebo effect does not occur; if the patient feels better, then they are better.
Considerations will be given to actual dosage shortly.
4. Vehicle. There are three options to choose from.
1. Thyroxin (T4)
2. Tertroxin (T3)
3. Dried, natural thyroid U.S.P
1. In this country Thyroxin (marketed usually as Eitroxin (Glaxo), is almost
invariably used. Of the naturally occur-ring thyroid hormones it is the chief.
The thyroid hormone in the natural state is made up of around 80% Thyroxine (T4)
15% Trilodothyronine (Tertroxin T3)
residual 5% Diiodothyronine
Mono idothyronine
Thyroxine works quite well for the more simple, uncomplicated, early, not
too severe, hypothyroid patient. But note should be made that this is not how
thyroid hormone is naturally produced. There is a body of opinion,
sympathetically supported by the writer, that if natural thyroid is not to be
used, then at least T4 should be combined with T3 for a more satisfactory and
more logical replacement.

2. Trilodothyronine - Tertroxin (T3). This is quite considerably more potent
than T4, four or five times so, but unlike T4, with an 8 day half life, the half
life’s about 8 hours. It is also fifteen times as expensive.

3. Dried Natural Thyroid. Used from about 1900, desiccated thyroid fell into
disfavour in this country and availability ceased in 1985. The synthetic
Thyroxine was considered to be a better, purer preparation. Though, of course,
it is purer - not containing the other thyronines - this may be its weakness;
and ignores the fact that thyroid replacement need not be exact. The amount
required varies from day to day, even hourly; and this dynamic variation may be
compensated for by the patient’s own thyroid - which although deficient, may
still be taking most of the load. It is widely used in USA, as Natural Thyroid
U.S.P., but in the U.K has to be specifically imported. It almost invariably
works better than the synthetic Eitroxin, and is generally preferred by patient.
About half of patients in the writer’s practice are maintained on this
preparation. (Gold Line Laboratories, Fort Lauderdale; or Armour thyroid, from
The Bames Foundation, Trumbull, Connecticut).

4. Conversion. Thyroxine has a low biologic activity, and is transported, linked
to a binding globulin in a non-active state. The removal of one of the four
Iodine atoms, from the Thyronine molecule, converts it to the biologically most
active Trilodothyronine (T3) - available as Tertroxin. This is achieved by the
(largely liver produced), 5 Diodase enzyme. In this form, it will be passed, via
receptors, into the cell, where passage of protein and sugars across cell
membranes is encouraged, and mitochrondrial activity stimulated. It is now clear
10 that prolonged and/or severe hypothyroidism may be associated with partial
failure of the 5-Diodase enzyme. Although suspected, this situation may be
diagnosed in default when failure of response in thyroid replacement occurs. The
effect of Thyroxine in this situation is to cause an overload of unused T4 due
to conversion failure. This will cause some symptoms of thyroid excess, high
pulse, tremor, headache for example, while the hyperthyroid symptoms remain (It
is of remark that on occasions, high T4 levels in this situation have resulted
in inappropriate hypothyroid medication, or thyroid ablation). Thyroid function
tests will show high FTI and low TSH; resulting in thyroid supplementation
actually being withdrawn by the physician.

Management, where this problem is believed to be present, consists in
discontinuing some or all T4 and substituting with T3, preferably in divided
doses. Since poor conversion may be associated with a raised sex hormone binding
globulin (SHBG) and high levels of exogenous oestrogen, re-appraisal of any HRT
may need to be considered. Ensuring correct levels of vitamins A & B, Iron and
Magnesium (as above), is also mandatory.

5. Receptor resistance or deficiency.
Resistance to the passage of T3 via the receptors has been seen in a number
of cases. Why this occurs is not clear, but long periods of thyroid dysfunction
are associated. The replacement dose of the chosen thyroid hormone has to be
much larger than usual, which may cause some heart searching. Deficiency results
from a protracted low thyroid state; prolonged low level desensitises the
receptors. This will improve with time, and treatment of any Adrenal
insufficiency present.
Adrenal Insufficiency
This might be more properly described as low adrenal reserve. Since
hypothyroidism adversely affects every cell, every tissue, every gland, in the
body it is clear that the endocrine system as a whole will be also similarly
affected. The adrenals will be subject firstly to lowered efficiency resulting
from a lowered vitality primary to hypothyroidism, and secondarily, to reduced
ACTH stimulation from the pituitary. As a result, in general, patients with a
protracted and / or severe hypothyroid state will have some degree of adrenal
insufficiency. A significant level of this will be suspected in these
1. Longstanding and severe hypothyroidism.
2. Episodes of extreme exhaustion, or collapse.
3. Bad response to minor illness.
4. Multiple allergies.
5. Digestive problems - Diarrhoea
Weight loss
6. Increasing arthralgia and morning stiffness.
7. Pallor, yellow pigmentation (due to poorly metabolised carotene)
8. Fainting, dizziness

These patients often present with dark rings under their eyes, looking quite
ill. Blood pressure is low, with a positive Raglan’s sign. (Pressure fails to
rise on standing). These symptoms and signs, it will be appreciated, are those
of the early phases of Addions Disease.
Estimation of blood Cortisol is usually unhelpful, but
De-hydroepiandrosterone sulphate (DHEA), the main hormone output from the
adrenals will be found to be low. Depressed levels in the endocrine system as a
whole are likely to be found. The low adrenal reserve means patients are more or
less well, until challenged by the stress of illness, (or life events) and the
replacement therapy itself initially, of thyroid hormone. And this partial
failure will affect adversely T4-T3 conversion; and the integrity of the thyroid
It is essential to manage this insufficiency where present, or where
suspected. Remarkably, patients with symptoms, signs and blood pathology of low
thyroid, may improve completely on management and correction of the adrenal
problems alone; as conversion and receptor efficiency improves, the thyroid
hormone circulating - partly unused - is brought into play.
Adrenal insufficiency is dealt with by the provision of the two hormones
most likely to be lacking; Cortisone/hydrocortisone, and DHEA.; (as pointed out
above, low DHEA may be used to infer low cortisone output). The treatment
therefore, is the exhibition of, ideally, Hydrocortisone. This should be given
in divided doses initially of 5mgm qds; after a week, lO mgm qds may be used.
This remains a physiological dose, not challenging or suppressing the adrenal
function, but supplementing it. In these doses all of the usual anxieties
associated with cortisone do not apply; since restoration of normality is being
aimed at.
This may need to be explained to patients long subject to media induced
fears of the horrors of corticosteroids. (Their physicians may share these
anxieties, unnecessarily,). Dr McCormack Jeffries’ papers on the subject are
most worthy of study. DHEA has reached prominence in recent times as a hormone
of multiple, and magic properties. Certain it is that the adrenals secrete more
DHEA than anything else, and the amount is inversly proportional to age. It is
metabolised to oestrogen and/or testosterone; but also has been shown to play a
role in reducing obesity; in reducing atherosclerosis and cholesterol; it
inhibits the glucose -6- dehydrogenase enzyme in cancer; it improves immune
response, and, possibly, acts as a neural facilitator. In physiological doses,
there seems to be no problem in its long-term use. If levels are demonstrably
low, it is reasonable to provide replacement therapy.

Treatment Protocol
1. General consideration. Correction of Nutritional deficiencies, and
elimination of environmental challenges and toxins, has been noted above.
2. Simple, early hypothyroidism. Readily available tablets of Eitroxin 50mg may
be used. Initial dose is low (in the elderly as low as 25mg daily) and will
usually start at 50mg daily. This may be increased 25mg daily every two or three
weeks. The ceiling is reached at the judgement of the physician with feedback
from the patient. It is unusual to go higher than 300mg.
3. Moderate hypothyroidism. If the synthetic products are to be used, many
patients will benefit if, when a dose of lOOmg or more is used, Tertroxin (T3)
is added. lOmg for each lOOmg of T4 is to be preferred, although this means
halving the standard 20mg tablet. The dose may be increased incrementally at the
physician (and patient’s) discretion.
If natural thyroid is to be used a start may be made with 1/2; grain.
(Commensurate with its 100 years of use by the medical profession, natural
thyroid is still measured in grains). Dosage is increased by 72 gr. every two
weeks; usually by six the dose will level off. Improvement on any given dose
continues for weeks and weeks; and the temptation, scenting victory, to increase
the dose too soon, should be resisted. (One grain equivalent 65mg of natural
thyroid is equivalent to 38mg T4 and 9mg T3). The definitive dose may remain
unchanged for months or years; but the patients should be allowed to make small
adjustments themselves, depending on activity, ambient temperature, for example.
4. Severe hypothyroidism. As indicated above, simple replacement is unlikely to
be sufficient. Receptor block and adrenal insufficiency require adrenal support;
preferably initiated a week before thyroid supplementation is started. A
satisfactory protocol is to, start with 5mgm hydrocortisone qds, and after a
week, double the dose. Alternatively Prednisolone 2.5 mgm (or the enteric-coated
Deltacortril) may be used, doubling after a week. Clinical judgment, based on
the patient’s condition being normal - perhaps after about three months - will
enable the dose then to be halved, and then discontinued. It will be a matter of
clinical judgment and preference to use T4 and T3 or natural thyroid.
Some patients already on thyroxine, but far from well, have to be considered
separately. If the condition is really quite severe, and increasing thyroxine
makes matters worse, it should 14 be stopped for a short while and cortisone
exhibited. The sudden improvement in thyroid uptake brought about by the
cortisone may actually result in overdose symptoms if exogenous thyroid is
continued. The treatment of choice is to restart thyroid hormone, using instead
T3, after a 7 day interim period; lO mg for a few days, then 20 mg and so on.
After the improvement is seen to be full, and sustained, Eltroxin (or natural
thyroid) can be re introduced. The general improvement may, secondarily, improve
endogenous thyroid production, which can result in the overall exogenous dose
being reduced.
As regards DHEA, its significance in the management of adrenal insufficiency
is unsure, but where low levels have been found, it seems proper and logical to
restore them to normality. In women 25mgm daily, and men 50mgm daily sometimes
produces significant benefit. In this practice, its use has always been an
The management of hypothyroidism in children requires fine clinical
judgement; but one quarter to one half of the adult dose seems to be a
satisfactory starting point. Reliance on blood testing should be modified by
clinical appraisal of the child and it’s parents observations. The diagnosis is
often missed in children; and should be considered in any child often ill. The
basal temperature test may prove a helpful pointer.
Thyroid insufficiency may have a number of different causes and its symptoms
may masquerade as a number of different illnesses. It should always be
considered in patient's with pro-longed ill health, and the diagnosis rely on
history and examination; the reliance of the profession on the pathological
tests in favour of thoughtful appraisal is to be deplored. The treatment is
inexpensive and low tech, requiring a few simple guidelines and a listening
approach by the physician. Rarely is consultant advice necessary; the family
physician is well able to initiate and monitor the treatment even in quite
severe cases. The rewards are invariable; with no fuss, and with delight, the
patients always get better. This common condition is one of few where simple
measures can transform patient's lives.

1. The Unsuspected Illness. Bames. Harper and Row. 1976
2. Jackson. A.S. Hypothyroidism. J.A.M.A. 165: 121: 1957
3. B. Durrant-Peatfield. Aspects Of A Common Missed Diagnosis. Journal
Of Nutrition And Environmental Medicine. 6: 4: Dee 1996
ORD W.M, On Myxoedema, a term proposed to be applied to anessential condition
in the critinoid infection observed in middle aged women. Transactions Of The
Medical - Chirurgical Society Of London
5. E. Hertzogue. Treatment Of Myxoedema International Clinic Week.
New York 4: 14: 1915
6. The Fallacy Of Thyroid Function Tests. The Riddle Of Heart Attacks.
Barnes & Barnes 1976. ROBINSON PRESS. ISSN 0-913730-27-0
7. Interindividual Differences In The Pituitary-Thyroid Axis Influence
The Interpretation Of Thyroid Function Tests. Clinical Endocrinology.
8. Staub et al. Spectrum Of Sub Clinical And Overt Hypothyroidism.
American Journal Of Medicine 92: June 1992 pp 631
9. Barnes. Temperature v Basal Metabolism. Journal Of American
Medical Association. 119: 1072, 1942
10. Klause Wenzel. Osteoporosis. Lancet 340 15. 8. 92 pp 435-6
11. Franhyn et al. Long-term Thyroxine treatment and bone mineral
density. Lancet 340 4.7.92
12. Jeffries. W.M. Safe Uses Of Cortisone. Charles C. Thomas. 1981
13. Klinefelter et al. Single Dose Prednisone Therapy. J.A.M.A. 241 No 25
14. Barnes. Etiology And Treatment Of Lowered Resistance To U.R.I.’s
Federation Proceedings 12 No I March 1953

Adrenal and gonadal function in hypothyroid adult male rats.

Tohei A, Akai M, Tomabechi T, Mamada M, Taya K.

Laboratory of Veterinary Physiology, Tokyo University of Agriculture and
Technology, Japan.

The functional relationship between thyroid, adrenal and gonadal hormones
was investigated using adult male rats. Hypothyroidism was produced by the
administration of 4-methyl-2-thiouracil (thiouracil) in the drinking water
for 2 weeks. Plasma concentrations of TSH dramatically increased, whereas
plasma concentrations of tri-iodothyronine and thyroxine decreased in
thiouraciltreated rats as compared with euthyroid rats. Hypothyroidism
increased basal levels of plasma ACTH and pituitary content of ACTH. The
pituitary responsiveness to CRH for ACTH release markedly increased, whereas
the adrenal responsiveness to ACTH for corticosterone release decreased.
These results indicated that hypothyroidism causes adrenal dysfunction in
adult male rats. Pituitary contents of LH and prolactin decreased in
hypothyroid rats as compared with euthyroid rats. In addition,
hypothyroidism lowered pituitary LH responsiveness to LHRH. Testicular
responsiveness to human chorionic gonadotrophin for testosterone release,
however, was not different between euthyroid and hypothyroid animals. These
results indicated that hypothyroidism causes adrenal dysfunction and results
in hypersecretion of ACTH from the pituitary gland. Adrenal dysfunction may
contribute to the inhibition of LHRH secretion from the hypothalamus,
possibly mediated by excess CRH.

PMID: 9014850 [PubMed - indexed for MEDLINE]

A case of congenital hypopituitarism: difficulty in the diagnosis of ACTH
deficiency due to high serum cortisol levels from a hypothyroid state.

Nanao K, Miyamoto J, Anzo M, Tsukuda T, Hasegawa Y.

Endocrinology, Metabolism and Genetics Unit, Tokyo Metropolitan Kiyose
Children's Hospital, Japan.

A three-month-old boy presented congenital hypopituitarism in which the
hypothyroid state masked ACTH deficiency. Multiple anterior pituitary
hormone deficiencies, including ACTH, were finally confirmed. High basal
serum cortisol levels (up to 45.1 microg/dl) were observed during a
stressful episode before L-thyroxine replacement therapy was started.
Decreased morning serum cortisol levels (5.0 microg/dl or below) were
observed on the sixth day of L-thyroxine replacement therapy despite mild
hypoglycemia (lowest serum glucose level of 50 mg/dl). ACTH deficiency was
then confirmed by insulin-induced hypoglycemia test (peak serum cortisol
level of 4.9 microg/dl). The present findings showed that serum cortisol
levels can be high during a stressful episode in an infant with ACTH
deficiency and a coexisting hypothyroid state. Thus, the diagnostic
evaluation of adrenal function soon after L-thyroxine replacement therapy is
important in order to verify a possible subclinical ACTH deficiency, even in
the presence of high serum cortisol levels before L-thyroxine replacement

PMID: 10426585 [PubMed - indexed for MEDLINE]

Here's one with no abstract available, but sounds very interesting!

1: Lakartidningen 1999 Feb 3;96(5):464-465 Related Articles, Books, LinkOut

[Increased level of TSH can be a sign of adrenal cortex failure. Not
necessarily thyroid gland disease].

[Article in Swedish] Sjoberg S, Werner S.Karolinska institutet, Huddinge sjukhus.
Publication Types:
Review, tutorial
PMID: 10064931 [PubMed - indexed for MEDLINE]


by Mary J. Shomon

The adrenal glands are small triangular-shaped endocrine glands,
located on the top of both kidneys. The adrenal gland is made up of
the medulla -- the center part of the gland -- which produces two
hormones, epinephrine and norepinephrine (also known as adrenaline).
Adrenaline is the "fight or flight" hormone that gives you a burst
of energy in a crisis. The gland is surrounded by the cortex, which
produces other hormones such as cortisone and androgens (male sex
hormones) such as DHEA androstendione. The adrenals also back up the
ovarian production of estrogen.

Extreme imbalances in adrenal function can occur...these include low
cortisol in Addison's Disease, and excess cortisol of Cushing's
Syndrome But these diseases are fairly uncommon. What is far more
common are subclinical imbalances in cortisol and other adrenal
hormones, in particular, fluctuations and problems in combination
with thyroid difficulties, that make finding the perfect hormonal
balance for wellness a sometimes difficult process of trial and

A number of physicians have been breaking ground in the area of
adrenal/thyroid interactions, including Barry Durrant-Peatfield,
M.D., the innovative UK doctor who has been the victim of a targeted
anti-alternative medicine campaign in England, and Washington, DC
area practitioner, Bruce Rind, M.D..

The adrenal/thyroid connection is also discussed in the new book,
published early June, 2001, by Richard and Karilee Shames, called
Thyroid Power. Richard Shames, M.D. graduated Harvard and University
of Pennsylvania, did research at the National Institutes of Health
with Nobel Prize winner Marshall Nirenberg, and has been in private
practice for twenty five years. Dr. Shames practices holistic
medicine -- with a focus on thyroid and autoimmune conditions -- out
of Boca Raton, Florida, and has for twenty years been engaged in the
search for answers about thyroid disease. Karilee Halo Shames R.N.,
Ph.D., Dr. Shames' wife, is herself hypothyroid, and is a Clinical
Specialist in Psychiatric Nursing and a Certified Holistic Nurse
with a PhD. in Holistic Studies. The Drs. Shames, who have been
interviewed here frequently before, have some interesting thoughts
to share with thyroid guide Mary Shomon about the adrenal/thyroid

Mary Shomon: Is there an important adrenal component to optimizing
thyroid treatment for patients?

Drs. Shames: If you have been prescribed the proper amounts of
thyroid hormone -- perhaps with additional substances to balance
your reproductive system -- and all is working well, you do not need
attention to your adrenal glands. If, on the other hand, you are not
doing as well as you'd like, and especially if your symptoms have
been somewhat atypical all along, then other factors need to be
considered. One of the most important additional factors to take
into account is your adrenal hormone level.

Mary Shomon: Can you tell us a bit more about what the adrenal
glands actually do?

Drs. Shames: Your adrenal glands are two tiny pyramid-shaped pieces
of tissue situated right above each kidney. Their job is to produce
and release, when appropriate, certain regulatory hormones and
chemical messengers.

Adrenaline is manufactured in the interior of the adrenal gland, in
an area called the adrenal medulla. The adrenal medulla is
stimulated directly by nerves from the sympathetic portion of the
autonomic nervous system, which regulates fight or flight.

The human body is organized so as to be able to respond immediately
to threatening situations by generating a tremendous amount of
energy in a hurry, which enables the person to run away quickly, or
face the threat and fight it with a massive influx of chemical
support. These chemicals increase blood pressure, heart rate, and
blood flow to muscles, while mobilizing sugar to burn. Nerve
impulses from the brain cause the release of adrenaline from the
adrenal gland, which helps you react appropriately in immediate
short-term stress situations (the "fight or flight" response).

Cortisol, the another chemical from the adrenal gland, is made in
the exterior portion of the gland, called the adrenal cortex.
Cortisol, commonly called hydrocortisone, is the most abundant --
and one of the most important -- of many adrenal cortex hormones.
Cortisol helps you handle longer-term stress situations.

In addition to helping you handle stress, these two primary adrenal
hormones, adrenaline and cortisol, along with others similarly
produced, help control body fluid balance, blood pressure, blood
sugar, and other central metabolic functions.

Mary Shomon: Can you explain how proper adrenal function might be
related to a patient's thyroid problem?

Drs. Shames: A major connection exists between low thyroid and low
adrenal. Low adrenal, also called adrenal insufficiency, can
actually cause someone's thyroid problem to be much worse than it
would be otherwise.

Correction of low adrenal is similar to correction of low thyroid.
You merely take a pill that contains some of the hormone you are
lacking. In the case of low thyroid, you obviously take thyroid
hormone. In the case of low adrenal, you simply take some adrenal
hormone. Chapter 7 in Thyroid Power assures you that doing so, when
appropriate, is not only safe and effective, but it can change your
life for the better.

Cortisol is in the category of medicines called steroids, a class of
body substances that derive their name from the fact that they are
built upon the structure of the common cholesterol molecule. Both
health practitioners and the lay public have great concern about the
safety of taking oral steroids.

We would like to address this issue directly by making a distinction
between high-dose steroid therapy and low-dose adrenal

What we are talking about is the use of small amounts of natural
adrenal hormone (hydrocortisone) to bring slightly low adrenal
function up to its proper normal daily range. This is in stark
contrast to the high doses of powerful synthetic adrenal hormones
commonly used to treat severe health problems, or to assist in
building muscles.

Mary Shomon: Why is it important for people who are hypothyroid to
know the levels of their adrenal hormones?

Drs. Shames: Adrenal insufficiency symptoms include: weakness, lack
of libido, allergies, dark circles under the eyes, muscle and joint
pain, dizziness, low blood pressure, low blood sugar, food and salt
cravings, poor sleep, dry skin, cystic breasts, lines of dark
pigment in nails, difficulty recuperating from stresses like colds
or jet lag, no stamina for confrontation, tendency to startle
easily, lowered immune function, anxiety, depression, and premature
aging. Some of these symptoms are similar to those of low thyroid.

If low-thyroid people with these symptoms are put on thyroid hormone
alone, they sometimes respond negatively. These people may have
coexistent, but hidden, low adrenal function. If they take thyroid
hormone by itself, the resultant increased metabolism may accelerate
the low adrenal problem.

The addition of thyroid hormone in this situation unmasks the also
disturbing low adrenal situation. The proper approach in this case
is to treat the patient with thyroid and adrenal support

Adrenal insufficiency, especially when unmasked by the addition of
thyroid hormone, is unpleasant and uncomfortable. To compound the
problem, the doctor and patient then may wrongly assume that thyroid
replacement has been a mistake. A tremendous opportunity for better
health has now been missed.

While uncomfortable, this dilemma can become a diagnostic tool. The
doctor could then gradually add thyroid and adrenal hormone
together, with the patient eventually taking optimal levels of both.
This careful attention and delicate calibration are demanding on the
practitioner and patient. Nevertheless, we have seen patient after
patient dramatically improve with such dedication.

Also, interactions between your hormones are sometimes as important
as the direct action of the hormone itself. Some adrenal hormones
assist in the conversion of T-4 to T-3, and perhaps assist in the
final effect of T-3 on the tissues. Some scientists believe that
even the entrance of thyroid hormone into our cells is under the
influence of adrenal hormones. Thus, if your adrenal level is low
enough, you might do well to take both adrenal and thyroid hormone

Mary Shomon: Some patients have reported that tests have shown high
cortisol levels, or that their problem is that the adrenals are too
high. Is the real problem one of excess of deficiency?

Drs. Shames: A failing adrenal gland goes through a hyper phase
before it becomes totally exhausted. In the 1950's, the famous
researcher Hans Selye divided the physiology of fight or flight into
three phases. In the first phase, "adaptation," a person
intermittently secretes slightly higher levels of the fight or
flight hormones in response to a slightly higher level of stress.

The second phase, called "alarm," begins when the stress is constant
enough, or great enough, to cause sustained excessive levels of
certain adrenal hormones. This can be the very earliest glimmer of
what later can become stress-induced illness.

The third phase is called "exhaustion," wherein the body's ability
to cope with the stress is now depleted. At this point, adrenal
hormones plummet, from excessively high to excessively low. It is
this latter phase of adrenal exhaustion that sometimes accompanies,
or is confused with, low thyroid.

Where do low thyroid and adrenal stress intersect? If you find
yourself in the alarm phase of adrenal stress (high levels of ACTH
and high levels of cortisol), one result might be altered conversion
of T-4 into T-3, or thyronine. Thus, your adrenal situation might
profoundly affect the availability of biologically active thyroid

Research shows that even success and positive change can result in
the stress response described above. In other words, even activities
that you perceive as enjoyable, such as working hard on an exciting
project, or striving for and receiving a promotion, can be perceived
by the body as stress. This positive stress, called "eustress," can
accumulate and affect bodily responses in the same way as its
negative counterpart, "distress." In addition, some of the
activities that are encouraged to help relieve this situation might
actually make it worse, as in the following example.

Mary Shomon: How would a low thyroid person determine if he or she
were low adrenal?

Drs. Shames: It would be wonderful to have a simple, reliable method
of assessing a person's adrenal function. Many tests are available,
but none are widely used. One reason for this is that most medical
doctors consider that the adrenal system is always functioning
smoothly, except in two very severe and rare circumstances. One of
these is caused by extreme excess adrenal function, and it is called
Cushing's Syndrome. When there is extreme decreased adrenal
function, this is called Addison's Disease. When it is clear to a
physician that you do not have either Cushing's or Addison's, the
topic of adrenal metabolism all too often is shoved aside.

Another reason why doctors may not be sufficiently involved in this
topic is that adrenal tests are even more challenging to interpret
than thyroid tests. The biochemistry is extremely complex, and,
until recently, the testing technology had not been useful except to
diagnose Cushing's and Addison's, the two main types of adrenal
problems. Now the measurements are more sophisticated. Current
technology can be divided into roughly two camps: conventional
medical evaluation; and the more recently developed alternative
adrenal tests.

Mary Shomon: What exactly are the conventional options?

Drs. Shames: The conventional medical evaluation for adrenal
function includes measurements of ACTH (adrenocorticotropic hormone)
from the pituitary, as well as cortisol (hydrocortisone) from the
adrenal glands themselves. Both of these are simple blood tests.

In addition, doctors will sometimes obtain a 24-hour urine sample
for cortisol and related cortex hormones. This involves having
patients collect urine in the same large container every time they
empty their bladder for an entire 24-hour period. One drawback with
this measurement is that it is not illustrative of variations within
the 24-hour period, because the whole day's worth of urine is mixed
together in one bottle. The level of adrenal hormone is naturally
high in the morning, progressively diminishing through the
afternoon, reaching its lowest levels in the evening. In the case of
the 24-hour urine sample, the doctor can determine if the total
amount of hormone is high or low for the whole day, but will not
know at what time of day major variations occurred.

Also, a normal level for 24 hours might mask very high levels at one
point in the day, with very low levels at another part of the day.
The total for 24 hours would be normal, but the patient may go
through half the day with excessively high levels, and the other
half excessively low. Complicating this test is the fact that the
blood cortisol level is dependent on the protein molecule that
carries it around in the bloodstream. The amount of this molecule
can change for a variety of reasons, which changes the level that is

Complicating this test is the fact that the blood cortisol level is
dependent on the protein molecule that carries it around in the
bloodstream. The amount of this molecule can change for a variety of
reasons, which changes the level that is measured.

Liver trouble can lower the amount of this carrier protein, which
will alter your test result. Abnormal estrogen levels will also
alter the amount of this protein. In addition to all this, one's
level of activity can change the result of the test.

The person's stress level has a significant impact too. Someone may
have rushed to get to the lab or come from a stressful meeting at
work. That would yield a different level than a patient who was
calmly sitting in the waiting room for half an hour before the test.
In addition, the conventional tests have a normal range that is very
wide, so that only the most severe, out-of-range abnormalities
qualify as being diagnostic of abnormal adrenal function (sound

For these reasons, many doctors do not order adrenal tests at all.
If they do, they generally focus not on cortisol, but on evaluating
adrenaline levels. You should tell your doctor that you would like
the cortisol testing, and that you want both a "free" and a "total"
cortisol level. The free fraction is available in more
recently-developed tests, and has more revealing information for
thyroid sufferers.

Mary Shomon: What tests are patients likely to be able to obtain
from more alternative or complementary practitioners?

Drs. Shames: Conventional medicine's evaluation of mild adrenal
insufficiency is stymied by the adrenal system's subtleties. What do
the alternative practitioners have to offer? They have chosen
laboratories that try to assess adrenal function somewhat
differently. A number of labs will do urinary measurements as
described above, but instead of using 24-hours' worth of urine, they
use four separate samples collected at 8 A.M., noon, 4 P.M., and
midnight. Testing four different samples taken throughout the day is
an attempt to obtain a more complete adrenal profile than one sample
would provide. This allows a more detailed picture of the patient's
daily cyclic adrenal function, and better distinguishes between
alarm the alarm phase and the exhaustion phase.

In addition to increased determinations per day, the new test
measures more than cortisol levels. Also commonly tested is DHEA, a
precursor to almost all the other adrenal hormones. (A precursor is
a chemical that is not as far along on the chemical pathway chain as
the final product.) The resulting set of numbers, which some labs
call the Adrenal Stress Index or ASI, can be then be used to
initiate and monitor therapy.

Saliva measurement is another type of test not yet considered part
of a conventional adrenal workup. The determination of hormonal
levels in saliva is, however, being researched for its effectiveness
in assessing glandular health and balance. One such saliva test is
similar to the urinary ASI above. It tests four saliva samples,
collected at four specific times of day (8 A.M., noon, 4 P.M., and
midnight). Like the urinary tests just mentioned, more than cortisol
levels are measured. Some saliva labs will check cortisol, DHEA, and
pregnenolone. Pregnenalone, like DHEA, is a chemical precursor to
many of the important adrenal hormones. The saliva measurement is a
good choice because of its ease of collection and affordability, but
its degree of reliability remains to be fully evaluated. Some
alternatitve practitioners are claiming improved success with
salivary testing.

Mary Shomon: Given these various options, what kind of adrenal
testing do you typically recommend for your patients?

Drs. Shames: We feel that the alternative testing of urine and
saliva, evaluating four separate samples in a 24-hour period, is the
preferred choice. It seems to reveal more of what is actually
occurring when a patient experiences disturbingly low points in his
or her day, or when proper thyroid treatment does not go well.
However, these alternative tests are unlikely to reveal the true
level of adrenal reserve.

Mary Shomon: How does one go about measuring adrenal reserve?

Drs. Shames: The method for measuring adrenal reserve has been
largely solved by a conventional medical test, the ACTH stimulation
test. Testing for adrenal reserve in this fashion is similar to the
definitive thyroid test of TSH reserve (TRH Test) described in Step
4 in our book, Thyroid Power.


Richard Shames, M.D. offers consultations by telephone, online or in
person at his holistic health center in Boca Raton, Florida. To
schedule an appointment, please telephone 561-417-7833. The same
services are available with Karilee Halo Shames, Nurse Health
Promotion Specialist, who teaches holistic nursing.


Dean_AdrenalAdrenal Maladaptation Syndrome:
A Sweet Solution For Coping With Stress
July 1998 Vitamin Research Nutritional News
by Ward Dean. M.D.
Stress is an a defining aspect of life in the 90’s—everybody has it, and
everybody talks about it, yet few people are able to define what stress really
is. Scientifically, stress is defined as the nonspecific response of the body to
any demand made upon it (Selye, 1974). When stress becomes excessive, is
damaging or unpleasant, we then properly refer to it as "distress."
Consequently, when we say someone is "under stress," we usually mean excessive
stress, or distress.

More important than finding a definition for stress is understanding the effect
it has on our bodies. Stress-producing factors, or stressors, can be physical
(work and exercise), biological (viral, bacterial and fungal), environmental
(heat and cold), and situational (job, family, etc). And while there are
numerous stressors, the responses they elicit from the body are very similar. It
may be difficult to accept that such essentially different things as cold, heat,
drugs, hormones, sorrow and joy could provoke identical biochemical reactions in
the body. Nevertheless, this appears to be the case. It can be demonstrated
scientifically that certain reactions to stress are totally nonspecific, and
common to all types of stressors. Emotional stimuli are probably the most common
stressors that most of us encounter in our daily lives—but they elicit the same
physiological response that an encounter with a saber-tooth tiger did for our
cave-man ancestors.

The Spice of Life
According to Professor Hans Selye, stress is "the spice of life." Certainly a
life free of stress and devoid of challenges would be filled with boredom and
hardly worth living. The most memorable events in life tend to be those that are
the most stressful—situations that require us to rise to a challenge and push
past our normal limits. Asks Selye, "Who would enjoy a life of no runs, no hits,
no errors?"

While it is important to recognize that excess stress can seriously affect human
health, certain types of stress are actually good for us and can benefit our
health. For example, most people today recognize the multiple physical and
emotional benefits to be gained from physical exercise. Physicians once treated
heart attacks with enforced inactivity. Now, we know that early resumption of
physical activity (stress) is often the key to a successful recovery. Clearly,
an issue for those looking to survive (and enjoy) the best in life is not how to
avoid stress, but how to best manage stress.

How the Body Reacts to Stress
1. Neuroendocrine Adaptation Mechanisms
A key factor in the maintenance of resistance to stress is the
hypothalamopituitary-adrenal axis (Figure 1). Stressors excite the hypothalamus
to produce adrenocorticotropic hormone (ACTH) which induces the adrenal cortex
to secrete glucocorticoids (principally cortisone) and DHEA, and the adrenal
medulla to secrete epinephrine and norepinephrine. When cortisone levels rise,
they inhibit the hypothalamus and pituitary, which in turn decrease CRH and ACTH
production, respectively. When blood cortisone levels decrease, hypothalamic
activity increases, releasing CRH. This increases pituitary ACTH output, which
stimulates the adrenal cortex to increase blood cortisone levels. In this cyclic
manner, equilibrium is maintained in the system.

Cortisone concentrations in the blood undergo cyclic, diurnal (circadian)
changes (Figure 2). These changes are due to variations in CRH and ACTH output,
as well as to changes in hypothalamic and CNS sensitivity to cortisol (these
changes in hypothalamic sensitivity are very important). With normal diurnal
rhythm, blood ACTH levels rise between 3 and 6 AM, causing increases in blood
cortisol. Thus, blood cortisol concentrations are at their highest in the
morning. These peak levels gradually decrease, dropping to minimal levels by
night. Under normal conditions, basal morning cortisol concentrations are twice
those at night.

Cortisone has been described by Dr. William Jefferies, author of Safe Uses of
Cortisone as "the hormone of life," as without it we would be unable to adapt to
the various stressors of life. However, when produced in excess over a prolonged
period, it has a number of adverse, damaging effects. These include elevations
of blood sugar, sodium retention (resulting in hypertension), suppression of
immunity, gastric ulcers, headaches, loss of bone density, and even heart

2. General Adaptation Syndrome (GAS)
The General Adaptation Syndrome (GAS) was first described by Selye in 1936. The
GAS involves three progressive stages (Figure 3). The first stage is the alarm
reaction, characterized by surprise and anxiety involved in dealing with a new
situation. During the alarm reaction, the adrenal medulla produces epinephrine
and norepinephrine—the "flight or fight" hormones. Also, the adrenal cortex is
stimulated to produce additional hydrocortisone and related hormones.

The second stage is that of resistance, where we learn to efficiently cope with
the stressor (adaptation). An ideal situation is one in which adaptation occurs
and continues until the stressful situation resolves, with a rapid return to the
resting state. However, just as any inanimate machine may wear out or break down
whenever a heavier load than it is designed to tolerate is applied, so too does
the human machine sooner or later become the victim of constant wear and tear.
Unfortunately, our capacity for adaptation is limited. Also, everyone’s
adaptational capacity (i.e., tolerance to stress) is different. What may "charge
one person’s batteries" may totally devastate someone else. Consequently, the
third stage of the GAS is that of exhaustion, involving a depletion of our
energy reserves and loss of adaptational ability, leading to fatigue, or other
symptoms or diseases. Just as a chain breaks at its weakest link, so too can
exhaustion of our adaptive capacity result in stress-induced disease. This stage
of adrenal exhaustion is also sometimes referred to as the adrenal maladaptation
syndrome, or hyperadaptosis (Dilman and Dean, 1992). Adrenal dysfunction may be
manifest by (1) an excess or inadequacy of cortisone, DHEA, ACTH and/or CRF; (2)
relative imbalances of these hormones and releasing factors, or (3) loss of
sensitivity of the hypothalamus and pituitary to the normal inhibiting effects
of these hormones.

Stress and Aging
As we mentioned previously, stress is the nonspecific response to any kind of
demand at any one time. The sum of all the stresses to which the body has been
exposed during a lifetime can contribute significantly to the ravages of aging.
A good example of the age-accelerating effects of stress is how President Jimmy
Carter literally aged in front of our eyes as he tried to cope with the Iran
hostage situation. The main difference between aging and The General Adaptation
Syndrome (GAS) appears to be that the GAS is more or less reversible if one is
provided with adequate rest or therapeutic intervention, using either
nutritional supplements or pharmaceutical drugs. But we must keep in mind that
as long as we live we are always under some measure of stress, and that although
excessive stress and aging may be closely related, they are definitely not
identical. Professor Vladimir Dilman, my co-author of the Neuroendocrine Theory
of Aging and Degenerative Disease (unfortunately, now out of print, but under
revision), said that Aging itself is a stressor.

Symptoms and Diagnosis
Individuals subjected to great stresses may develop adrenal maladaptation
syndrome. In these instances, the glands work beyond their capacity, passing
through the alarm reaction, the stage of resistance, and finally reaching the
stage of exhaustion. Adrenal maladaptation syndrome may cause a variety of
symptoms, depending on which organ system is the "weak link" in the chain. Some
of the most common symptoms are listed in Table I. Symptoms are often similar to
those found in persons who suffer from hypoglycemia, hypothyroidism, chronic
fatigue, and fibromyalgia. Prior to treating someone with thyroid for suspected
hypothyroidism, it is important to first determine whether there is some adrenal
involvement. Supplemental thyroid given to patients who are both hypothyroid
(low thyroid) and hypo-adrenal, who are not first provided with adrenal support,
will often suffer from a worsening of their symptoms. However, despite this
warning in the Physician’s Desk Reference ("Thyroid hormones are generally
contraindicated in patients with uncorrected adrenal cortical insufficiency."),
it is an extreme rarity for physicians to evaluate adrenal function prior to
prescribing thyroid hormone replacement.
Table 1*
Signs and Symptoms of Patients with Hyperadaptosis (Adrenal Maladaptation
• Fatigue
• Nervousness
• Severe PMS
• Salt craving
• Depression
• Inability to concentrate
• Carbohydrate craving
• Allergies (hay fever, asthma)
• Anxiety
• Headache
• Alcohol intolerance
• Muscular pain and tenderness
• Joint pains and tenderness (arthritis)
• Weakness
• Poor memory
• Palpitation
• Abdominal discomfort
• Alternate diarrhea and constipation
• Obesity
• Poor wound healing
• Glucose intolerance
• Moon face
• Purple striae
• Loss of bone density
*Tintera, 1955.

Diagnosis of the Adrenal Maladaptation Syndrome is usually based first on the
presentation by the patient with one or more signs and/or symptoms listed in
Table I. Often, treatment is initiated on an empirical basis, with no further
testing, since the treatment is relatively benign and the likelihood of
improvement so high. Although there are a number of blood tests that may
contribute to the diagnosis, recently an innovative salivary hormone test has
been developed that tracks not only the time-related changes of the levels of
DHEA and cortisone, but also the DHEAlcortisol ratio as well. This test provides
objective information on which to base the optimum therapeutic program.
Treatment of Adrenal Maladaptation Syndrome
While even scientists who have extensively studied the adrenal maladaptation
syndrome may disagree as to whether it is due to too much or too little
production of hormones from the adrenal cortex, or perhaps from too high or too
low production of ACTH or CRF—what these scientists do agree on is that all of
the symptoms are due to an alteration of the performance of the hypothalamus and
the adrenal cortex—and these apparently diverse conditions surprisingly often
respond to the same therapy.
First, in any condition characterized by adrenal dysfunction, I believe it is
extremely important to stabilize blood sugar—whether it is too high or too low—
thereby alleviating a major metabolic stress on the body. Consequently, I
generally recommend a "zone" type diet in these cases, i.e., one that emphasizes
protein and fat, and restricts the amount of carbohydrates—especially refined
carbohydrates. Also, I recommend numerous small meals or nutritious snacks
throughout the day.
Second, exercise is probably one of the best "stress fighters" there is, and
should be incorporated into the program. This does not have to be a six mile jog
or a session of heavy weight lifting. Even when fatigue is so extreme that it is
difficult to get out of bed, many people find that taking a walk around the
block has a tremendous energizing effect.

Third, nutritional and/or pharmocological support to restore (1) hormone balance
and (2) hypothalamic sensitivity to inhibition by glucocorticoids (cortisone).
Substances that may be of help to restore hypothalamic sensitivity include: (1)
phosphatidylsenne (100-300 mg per day); (2) Melatonin (750 mcg-6 mg per day at
bedtime); (3) Metformin (500 mg two-three times per day); and (4) Dilantin (100
mg twice per day). Substances that may directly alter hormone levels and balance
include: (1) Pregnenolone (10-100 mg daily in the morning); (2) DHEA (5-100 mg
daily in the morning); (3) hydrocortisone (5-20 mg daily in divided doses) or
glycerrhizin (25-1 00 mg daily—usually in the morning).

Provision of adrenal support by the use of (1) low-dose hydrocortisone treatment
(as outlined in Dr. William Jefferies’ book, Safe Uses of Cortisone, (2)
intravenous adrenal cortical extract, or (3) nutritional supplementation with
adrenal glandular supplements and/or glycerrhizin—a food additive nutritional
supplement that is extracted from licorice, which mimics the effects of
Glycerrhizin—Natural Cortisol-Mimicking Extract From Licorice
It has long been known that moderate consumption of licorice has beneficial
effects in a variety of diseases, including allergies, asthma, chronic fatigue,
hypoglycemia chronic stress, inflammatory conditions, and other symptoms that
are outlined in Table I. Glycerrhizin is the ingredient that is removed from
licorice—[DGL (deglycerhizinated Iicorice)]—that enables people to benefit from
the ulcer-healing properties of licorice without worrying about the dangers of
excess cortisone. Glycerrhizin is also the active ingredient in licorice which
mimics the effects of cortisone, and from which licorice’s beneficial effect is

Glycerrhizin (and its ~‘cousin ," Cortisone), however, are like two-edged
swords. In small to moderate doses, they can be very beneficial. In excess, they
can cause a number of adverse side effects, including water retention, elevated
blood pressure, and loss of potassium. Consequently, it is very important to use
the minimum effective dosage of glycerrhizin, and to use it intermittently as
needed (usually, for no more than 6-8 weeks at a time). Periods of use of
glycerrhizin should be interrupted by two to three weeks of non-use. Many people
find that taking 25-100 mg/day of glycerrhizin provides significant relief of
symptoms of chronic fatigue, fibromyalgia, and other conditions that are related
to "adrenal exhaustion" or adrenal maladaptation syndrome.

Many people find that taking 25-100 mg/day of glycerrhizin provides significant
relief of symptoms of chronic fatigue, fibromyalgia, and other conditions that
are related to "adrenal exhaustion" or adrenal maladaptation syndrome.

In order to mimic the body’s normal rhythm of cortisol, we recommend that
glycerrhizin be taken first thing in the morning, approximately 30 minutes
before breakfast, and another (usually smaller) dose (if needed) before lunch.
With glycerrhizin, as with many supplements—more is not necessarily better. Only
the minimum dose that produces the desired effect should be taken.

1. Barnhart, Edward R. Physicians Desk Reference, Medical Economics, Oradell,
New Jersey, 1991, 690.
2. Dilman, Vladimir, and Dean, Ward. The Neuroendocrine Theory of Aging and
Degenerative Disease, The Center for Bio-Gerontology, Pensacola, Florida. 1992.
3. Jefferies, William, McK. Safe Uses of Cortisone, Charles C. Thomas,
Springfield, Illinois, 1981.
4. Selye, Hans. Stress Without Distress. Signet, New York, 1974.
5. Tintera, John W. The hypoadrenal state and its management. New York State
Journal of Medicine, 55:13, July 1, 1955, 1-35.

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text remains intact, unchanged and with Vitamin Research Products, in, listed as
source. Commercial use or commercial distribution may not occur without the
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No information in this article should be taken as a recommendation. if you have
any questions about the relationship between Nutritional Supplements and your
health, seek the advice of a qualified physician.

Copyright 1996 -2000 Vitamin Research Products

From Pathguy:

THE ADRENAL CORTEX: "An organ essential to life."

Three "zones":
(1) Zona glomerulosa: mineralocorticoid production. Thin.
(2) Zona fasciculata: glucocorticoid production (?), resting cells (?).
(3) Zona reticularis: glucocorticoid production, androgen and estrogen
production, grossly darker than outer layers. Brown.
(Mnemonic: Salt, sugar, and sex: the deeper you go, the sweeter it gets.)
Under the microscope, the borders are fairly easy to see.
In newborns, the future adult cortex is a thin layer under the capsule, and
most of the gland is "fetal zone". This regresses in a few weeks.
Future pathologists:
The normal adult weight of each adrenal gland is 4 gm.
If an adrenal gland weighs 6 gm or more (without a tumor), it is usually
hyperplastic. The stress of the final illness increases the weight of the
adrenals, which is why "normal autopsy weight" is sometimes given at 6-8 gm.
Most violent suicides have adrenals weighing 9-11 gm (Am. J. Psych. 144:
1214, 1987; confirmed AJFMP 19: 72, 1998.)
* Future pathologists only: If the stress is very acute, expect lipid
depletion of the cortex. If the stress was a few days ago, look for lots
of lipid in the ZF, with none in the ZR or ZG.
* More for future pathologists: A bit of ectopic marrow, a few pigmented
cells, or theca cells (especially in menopausal women) are normal.
* Ask a physiologist about the role of dehydroepiandrosterone in health;
about 30% of a man's androgens are derived from this, and 90% of a
post-menopausal woman's estrogens.
{49431} hyperplasia of adrenal cortex, etiology undisclosed
{ 9217} adrenal cortical hyperplasia, etiology unknown
*Around 2% of patients have adrenals with black nodules, usually without any
evidence of dysfunction.
Two types, both uncommon:
(1) Anencephalic type: thin cortex, no fetal zone
(2) Cytomegalic type (X-linked recessive?): thin cortex composed entirely of
large, bizarre cells (foci of such cells are common in normal newborns but
regress). * The gene is DAX1, a nuclear hormone receptor (JAMA 274: 324,
1995); a milder allele produces late-onset adrenal insufficiency and
hypogonadotropic hypogonadism (J. Clin. Emd. Met. 86: 3171, 2001).
Both present as hypoglycemic seizures in infants. Glucocorticoid replacement
saves these children's lives.
ECTOPIC ADRENAL CORTICAL TISSUE (sometimes ectopic adrenal medulla too)
This is most common in the capsule ("capsular extensions") and at the origin
of the celiac artery, but it can occur anywhere in the retroperitoneum, or
under capsules of liver, kidney, ovary, or testis.
Ectopic adrenal caused problems when surgical adrenalectomy was very popular.
("A new adrenal gland grew back in a different place....")

HYPOADRENOCORTICISM ("Addisonism", etc.): Insufficient glucocorticoid (and
usually insufficient mineralocorticoid) production.

Chronic hypoadrenocorticism (Addison's disease, now regardless of etiology).
Troubles start when 80% of the gland tissue is gone. Review Br. Med. J. 312:
1085, 1996.
You need to know the etiologies of chronic hypoadrenocorticism:
Most of Dr. Addison's patients had bovine TB of the adrenals (by way of
the lymphoid tissue of the duodenum).

Worldwide, fungal infections (remember histoplasmosis, coccidioidomycosis
and South American Blasto) and leprosy are important causes, and now AIDS
is too.
The most prevalent non-iatrogenic cause of Addison's disease in the US
today. The adrenal remnants are typically loaded with lymphocytes, etc.,
etc. Jack Kennedy suffered from this illness in his youth, and it was
missed for several years (JAMA 201: 115, 1990).
Long-mysterious, it's now clear that most of these patients have
autoantibodies against 21-hydroxylase (Lancet 339: 1559, 1992).
Presumably this is antibody-dependent cell-mediated cytotoxicity, as in
Hashimoto's disease.
Autoimmune adrenalitis often occurs jointly with Hashimoto's
thyroiditis, type I diabetes mellitus, vitiligo, gluten enteropathy,
and/or pernicious anemia (* autoimmune "polyendocrine deficiency
syndrome II", "Schmidt's syndrome", etc.)
*There's a family of autoimmune polyendocrinopathies in which there are
various immune and non-immune disturbances and a curious inability to
keep candida from infecting mucosal surfaces. Type I (2 of 3
hypoparathyroidism, addisonism, mucosal candidiasis; there's often other
autoimmune problems too) has just yielded its secrets -- it's an
autosomal recessive, known locus APECED, which causes patients to make
an autoantibody against tryptophan hydroxylase (TPH): Lancet 352: 255,
1998). Surprised that an autoimmune disease can be simple-mendelian? I
This results from too-rapid withdrawal of glucocorticoid medication,
post-adrenalectomy for breast cancer or Cushingism, etc., ketoconazole
or fluconazole antifungal drug therapy (Crit. Care Med. 29: 668, 2001),
removal of a "non-functioning adenoma" (rare).
Others: Worth remembering are
congenital hypoplasia
hemochromatosis (a common disease under-diagnosed in the U.S.)
metastatic cancer to adrenal glands (can cause Addisonism, see Cancer
65: 177, 1990).
anticoagulant therapy (bleeds into the adrenals; NEJM 321: 1595, 1990)
CMV infection (in AIDS, it's almost the rule; Am. J. Clin. Path. 93:
651, 1990).
adrenal leukodystrophy (very long-chain fatty acids accumulate;
"Lorenzo's oil"; ask a biochemist, neuropathologist or geneticist; gene
located Nature 361: 726, 1993); J. Clin. End. Metab. 81: 470, 1996
describes the forme-fruste with Addison's but no neuro problems; this is
perhaps common J. Clin. End. Metab. 81: 470, 1996.

Adrenal amyloidosis NOTE: Hollywood is Hollywood. Evidence that "Lorenzo's oil" benefits
adrenoleukodystrophy patients remains "anecdotal" (Brain & Dev. 14: 409,
1992); it failed controlled studies miserably (NEJM 329: 745 & 801, 1993;
NEJM 330: 1904, 1994; Ann. Neuro. 34: 121 & 169, 1993), and poisons
platelets (NEJM 328: 1126, 1993; Am. J. Hem. 44: 290, 1993; J. Inh. Metab.
Dis. 17: 628, 1995) and (at least sometimes) natural-killer lymphocytes (J.
Inh. Metab. Dis. 18: 101, 1995). We've now got two series of dead
adrenoleukodystrophy patients who were treated in life with Lorenzo's oil.
It turns out that the stuff doesn't even cross the blood-brain barrier,
which is probably why it doesn't work (Neuroch. Res. 19: 1073, 1995; Ann.
Neuro. 36: 741, 1995).
ACTH deficiency ("secondary hypoadrenocorticism")
These patients have almost always lost their adenohypophysis and have
"panhypopituitarism". (Treat the whole person.... Caring for a little
pituitary dwarf? Don't get focused on the height so that you forget the
likely adrenal insufficiency.... J. Clin. End. Metab. 81: 1693, 1996) Less
often, they have selective, presumably autoimmune, loss of the
ACTH-producing cells: Arch. Int. Med. 152: 1705, 1992.
Clinical picture:
"Addisonian" patients show weakness, nausea, and weight loss, and are
usually hypotensive (* 110/70 or less) and have other complaints. Like most
endocrine patients, the problems are likely to appear "emotional".
In primary hypoadrenocorticism, the skin and buccal mucosa will usually be
hyperpigmented, due to increased ACTH (MSH?) -- also look at freckles,
nipples, palmar creases, old scars.
Lab studies typically show hyponatremia, hyperkalemia, metabolic acidosis,
hypoglycemia, low serum cortisol, low urinary 17-OH-steroids, and (most
important) failure to respond to various "stimulation tests" by increasing
cortisol output.
It is common for these patients to die suddenly and unexpectedly before
anyone thinks of adrenocortical insufficiency. This still happens (Br. Med.
J. 312: 1085, 1996).
*Osteoporosis is severe in post-menopausal women with Addisonism, because of
loss of adrenal androgens.
Replacement therapy is life-saving. (And get your patient a syringe of
cortisol and an ID bracelet.)
* Some women feel better and have better sexuality if they get some DHEA.
Makes sense. Why? (NEJM 341: 1013, 1999).
{ 9371} Addison's disease; pigmentation and vitiligo (mother and daughter)
{ 9372} Addison's disease, face
{ 9373} Addison's disease, buccal pigmentation
{49438} Addison's disease, pigmentation
{49439} Addison's disease, pigmentation
{49440} Addison's disease, atrophy of the adrenal gland
Selective hypoaldosteronism is rarely due to primary disease of the adrenal
cortex. (Clinicians talk about "hyporeninemic hypoaldosteronism".)
Much more often, the problem is really that the JGA is not producing renin
(REE-nin, remember?). Usually the problem is diabetic arteriolar disease (no
surprise); less often, it is one of the diseases of the renal tubules and/or
*These patients have type IV renal tubular acidosis, exhibit normal response
to ACTH stimulation testing, and need a prescription for oral
Acute hypoadrenocorticism ("adrenal apoplexy", "Addisonian crisis"): Sudden
collapse, often fatal (the mechanisms are not fully understood, but it
involves opening of the peripheral vasculature and shock with high cardiac
output; consider giving any such patient glucocorticoid: Arch. Surg. 128: 673,
It may result from undiagnosed adrenal insufficiency (iatrogenic, or
patients stressed by infection, surgery, or treatment of concurrent
myxedema; see for example J. Traum. 32: 94, 1992), or from known Addison's
disease when extra glucocorticoids are not provided during stress.
Waterhouse-Friderichsen syndrome ("adrenal apoplexy") features hemorrhage,
fibrin thrombi, and sometimes necrosis in the adrenals in a setting of
sepsis. It's not clear whether death is due to adrenal shutdown, but it's
not helping.
This occurs when there is overwhelming sepsis with hemorrhage into, and
destruction of, the adrenals. Patients develop purpura, shock, and die in
a few hours.
The etiologic agent is classically N. meningitidis, though staphylococci,
pneumococci, and H. influenzae are other important causes.
W-F is not rare, and is often overlooked. One group suggests that if your
patient in shock does not have elevated serum cortisol, he or she
presumably has W-F. Draw blood, then give 200 or 300 mg of hydrocortisone
(West. J. Med. 150: 582, 1989). Another protocol, for anybody who's
septic: Am. J. Med. 98: 266, 1995.
{24606} Waterhouse-Friderichsen adrenal, gross
{ 9224} adrenal hemorrhage, consistent with Waterhouse Friderichsen
{ 7570} adrenal hemorrhage, gross, consistent with Waterhouse-Friderichsen
The aphorism -- "A physician is only as good as his index of suspicion" -- is
especially applicable to endocrine disease. As an alert clinician, you will
often suspect adrenal gland problems and will want to order sensitive tests.
Some classic cases:
the thin, tired patient who has no appetite: Addison's disease?
Order a rapid ACTH ("cosyntropin") stimulation test
the patient who is gaining weight and who is depressed, has high blood
pressure, has hyperglycemia, or has one of many other problems: Cushing's
Order serum cortisol determinations at 8 AM and 8 PM (circadian rhythm is
always lost in Cushingism), plus a low-dose dexamethasone suppression
test, or just order a 24 hr urinary free cortisol.
the patient with high blood pressure and low serum potassium: aldosteronoma?

Measure urine aldosterone; check to see if plasma aldosterone fails to
increase on standing up; consider performing a saline infusion
aldosterone-suppression test or e a CT or isotope scan.
the lady who's starting to grow a mustache: late-onset congenital adrenal
Administer ACTH and measure blood 17-OH-progesterone.
the nervous patient with high blood pressure and headaches:
Check serum/urine catecholamines and/or metabolites, ask your lab.
Of course, only some of these patients are endocrine cases. As a rule,
meaningful hormone assays are performed under conditions of attempted
stimulation (if you suspect deficiency) or attempted suppression (if you
suspect over-production). If your screening tests are positive, or if you have
any doubts, get consultation. (One problem is that reliable, cheap plasma ACTH
assays are still not routinely available.)
If you diagnose endocrine disease which is not present, the patient gets
lifelong medication, unnecessary surgery, or unnecessary radiation. If you
fail to diagnose a disease which is present, the patient is likely to die of a
disease which might have had an excellent prognosis. (Suicide is common among
patients with Cushing's syndrome.) If you make the correct diagnosis, the
treatment of endocrine disease is very satisfying to physician and patient
alike -- because it works.


Dr. David Williams April 18, 2001

Hypoadrenia self-test

Do You Have Low Adrenals?

The adrenal glands are two small glands that sit directly
above the each kidney. They produce numerous hormones
essential to life. A few of the actions performed by these
hormones include:

regulation of blood sugar levels
controlling blood pressure
helping to provide resistance to stress
fighting the blood vessel enlargement, swelling and
fever associated with inflammation. Hormones produced by
the adrenals are the body's natural anti-inflammatory compounds (cortisone).
producing both male and female hormones in everyone, regardless of sex

What is hypoadrenia?

Hypoadrenia (low adrenals) occurs when the glands are not
quite capable of meeting all of the demands on them.

If you have the condition called hypoglycemia (low blood
sugar), you will almost always have hypoadrenia along with it.

When blood sugar levels drop (usually from the roller coaster
effect of eating refined sugar), the adrenals must work
overtime by producing hormones that tell the liver to convert
proteins to glucose to raise the blood sugar levels back to

Eating sweets depletes the adrenal glands. That's why you need
to follow a good diet and nutritional program.

Symptoms include:
dizziness (especially when standing)
constant fatigue
varicose veins
swelling in the ankles, feet or hands
chest pains

Hypoadrenia self-test

Hypoadrenia is not normally found in standard laboratory
testing; however, it is easily recognized by doctors familiar
with the condition. If you have a blood pressure cuff at home
and know how to use it, you might try the following screening test:

1.As you lie on your back, have someone record your blood pressure.
2.Quickly sit upright and have your blood pressure taken again.
3.After standing up, take your blood pressure again.

Normally, with the help of your adrenal glands, your blood
pressure will rise between 4 and 10 points (mm/Hb) when going
from the lying to standing position. If your blood pressure
drops, it may be an indication of hypoadrenia.

Naturally replenishing adrenal glands

To strengthen your adrenal glands, several areas need to be
addressed. Along with exercise and eliminating sugar from your
diet, include the following nutritional support:

Vitamin C: 2,000 to 5,000 mg daily
Vitamin B-complex: 1 B50 or B100 high-potency tablet daily
Pantothenic acid: 250 to 2,000 mg daily
Malic acid and magnesium are two components that have
been found to aid in converting fat and sugar into

You should be able to find several malic acid and magnesium
products in your local health food store. Recommended dosages
will be listed on the label and may vary, depending on the
strength of each product.


Just a case study, but might give you some ammunition...

: Endocr J 1998 Jun;45(3):385-391 Related Articles, Books, LinkOut

Reversible hypothyroidism in empty sella syndrome: a case report.

Otsuka F, Ogura T, Hayakawa N, Harada S, Kageyama J, Makino H.

Department of Medicine III, Okayama University Medical School, Japan.

A 33 year-old Japanese woman complained of generalized fatigue, recurrent
infections and gradual weight loss 1 year after her first delivery. During
delivery, no excessive bleeding or change in blood pressure was noted. On
endocrinologic examination 2 years after delivery, she was found to have
severe adrenal insufficiency and hypothyroidism. Pituitary function tests
revealed impaired responses of ACTH, PRL and gonadotropins, and normal
response of GH. TSH response to TRH was delayed but not exaggerated. Cranial
magnetic resonance imaging showed an empty sella. The adrenal glands were
responsive to extrinsic ACTH, and adequately accumulated 123I-aldosterol.
Antipituitary and antithyroid autoantibodies were detected in her serum. She
was diagnosed with partial hypopituitarism associated with empty sella
syndrome. Approximately 2 months after administration of cortisone acetate
25 mg/ day her general condition was noticeably improved, with normalization
of thyroid function and improvement of gonadotropin responses to GnRH. This
case suggests that a physiologic dose of glucocorticoid is necessary to
maintain not only thyroid function but also some of the remaining pituitary
functions in patients with empty sella syndrome manifesting hypopituitarism.

PMID: 9790274 [PubMed - indexed for MEDLINE]


Well, if you want to test to ensure you don't have adrenal problems and your
insurance will pay for it, I don't see what the doctor's problem would be. I
mean, doctors should test for this anyway. It says very clearly on the
Armour thyroid insert: "CONTRAINDICATIONS: Thyroid hormone preparations are
generally contraindicated in patients with diagnosed but as yet uncorrected
adrenal cortical insufficiency, untreated thyrotoxicosis, and apparent
hypersensitivity to any of their active or extraneous
constituents....Thyroid hormone therapy in patients with concomitant
diabetes mellitus or diabetes insipidus or adrenal cortical insufficiency
aggravates the intensity of their symptoms." If adrenal problems are there,
maybe they are slight, but continual increases in thyroid hormone to get
your lab results normal and make symptoms go away will only worsen the
adrenal state. I believe this is what has happened to me, as my numbers look
right, I have had to switch to Armour for the t3/t4 combination and still
have lingering symptoms, allergies and fatigue. These are directly linked to
adrenal fatigue (not necessarily insufficiency) and when I started taking
Enzymatic Therapie's Adrenal Cortex supplements I noticed a definite
difference. My thyroid doc, who is excellent, said I don't have adrenal
insufficiency or failure because that condition would be immediately
apparant--it would hit her as soon as she saw me. My counter argument was
that I don't think I have a failure or insufficiency either--I believe that
I have a situation where my adrenals are easily stressed, moreso than a
normal person, and where a normal person might have, figuratively, a
"gallon" of adrenal reserves, I may only have a "half-gallon" and then the
symptoms start. I've only been diagnosed with thyroid for about 2 years now,
but I've had allergies, athsma, skin sensitivities, low athletic abilty, etc
for as long as I can remember. Occassionally, I would get huge attacks that
docs would treat with a 10 day run of Prednisone, which worked like a
miracle--all symptoms vanished and I felt wonderful. This is the argument I
used to convince them to run the full adrenal testing on me, once the
insurance kicks in.


DHEA comes almost exlusively from the adrenals in women, and secretion
is stimulated by ACTH from the pituitary. Since ACTH also stimulates
cortisol production, having a normal (albeit from a relatively unreliable
saliva test) cortisol level and a high DHEA is a strong indication for
PCOS. What might help would be DHEA-S (or could be called DHEA-sulfate)
and testosterone results. If testosterone is normal, then the DHEA must
have come from the adrenals. A condition called CAH, congenital adrenal
hyperplasia, can also show high DHEA without increased levels of cortisol.

R. wrote:
> I have questions about two adrenal tests thusly:
> 1. I had the dexamethasone suppression test some weeks back - I took
> two small pills at 11.30pm, then had blood drawn the following morning
> at about 9am. I gather that this was to test for Cushing's. The day
> I took the dex pills, I felt typically ghastly - exhaustion, pain,
> misery, jitteriness etc. But the following day (the day I had the
> blood drawn) I felt a great deal better.
> When I saw the horrid endo for the results of the tests about ten days
> ago, the first thing that happened was that he asked me if there had
> been any change, and I told him about this. He said it was
> interesting and then seemed to ignore any implications.
> Post-dex, the result should apparently be below 200. Mine was 29.
> So my question is what the dexamethasone suppression test is, and what
> the possible results might be, and what they might mean. If it
> suppresses cortisol production, why would that make me feel better
> (especially if I'm not producing much on my own) or was that just
> coincidence?

The dexamethasone suppression test is used to test for Cushing's to see
if one has overactive adrenals, the body producing too much cortisol.
"Dexamethasone is a synthetic steroid similar to cortisol, which
suppresses ACTH secretion in normal people; giving dexamethasone should
reduce ACTH levels resulting in decreased cortisol levels." So if you
were producing too much cortisol, and the dexamethasone does not lower
the cortisol level as it should, you have overactive adrenals, which
could be Cushing's. This did not happened, it did reduced your cortisol
level, all it proved was that you don't have overactive adrenals. But,
it didn't test to see if they are under active.



IMHO, if your body was low on cortisol, the dexamethasone may have made
you feel better because it was giving you a replacement dose. It gives
a replacement dose, then it indirectly effects the cortisol level,
suppressing ACTH, which in turn lowers your own bodies output of
cortisol for a short period of time (5 mg of dexamethasone suppresses
the hypothalamic-pituitary-adrenal (HPA) axis for 2.75 days). How did
you feel a day or so later after the dexamethasone wore off???
(Dexamethasone is considered a long-acting glucocorticoid - .75 mg has a
half-life of 36-54 biologic hours which is longer than the short-acting
hydrocortisone: 20 mg = 8-12 hours or intermediate-acting prednisone: 5
mg = 18-36 hours).



The test that should been done for adrenal insufficiency (AI) is the
ACTH stimulation test. Cortisol level taken prior to an injection of
ACTH. The ACTH should cause the cortisol level to rise, if not you have AI.



> 2. Today I'm doing the Adrenal Stress Index test with four saliva
> samples at 8am, noon, 4pm & midnight. Unfortunately, when my doctor
> was telling me about this, I felt quite overwhelmed & didn't take much
> in. I gather it tests more than one thing. Can anybody please tell
> me what it tests & what different results might mean? A reference to
> a wedsite explaining these would be welcome.

This site is useful in explaining what's being tested and such.


This has 4 sample tests with interpretation.


This page shows a normal chart with a link to the next phase. Each key
has a link to the next one at the bottom.


Then the chart for ASI correlation.


> I really, really hope the ASI shows something. I *know* my adrenals
> are scragged.

I haven't had an ASI saliva test done, but the ACTH stim test showed
that I have AI. My cortisol level prior to the ACTH injection was less
than 0.2 and after it only rose to a 3. (Normal would have been rising
to 18 to 20 since I see you have a different scale). This had been done
in the afternoon and when a prior 8 am cortisol reading had been taken,
it was less than 1. So if this has any correlation to an ASI test, I'm
at the 7th Phase - "Adrenal is in a state of near complete failure!!!"

Jen wrote:
> Sara, Ted, others, etc,
> I've read the adrenal fatigue stuff on drrind.com again, trying to find an
> answer to my sugar difficulties.
> I find that in most cases I can circle the options under the 'adrenal'
> column, and the blood readings suggest that my thyroid condition was not
> primary, but secondary. Secondary to what, I'm not sure. Adrenal problems
> probably since I'm always so stressed out. I've been in a non-stop stress
> attack for years now, it is unrelenting.
> So. If i was to assume that this was my problem, or try to run with that
> info, whats the best way to sort it? Besides the obvious, which is to get
> the blood tests run, your GP has to believe you first in order to order them
> up, and so far no one even believes hypoglycaemia is real, let alone
> treating adrenal fatigue in the UK!!! And the queue to see my own GP
> stretches into Feb now, I can't go unless I'm armed with facts anyways.
> Knowing what happened to Dr D-P in the UK,

Are you referring to Dr Barry J Durrant-Peatfield? Why, what happened
to him???


I found good info from his site which lead me to answer why I could not
tolerate taking thyroid meds.

I don't know if the saliva test can be done in the UK.


I haven't had the saliva ones done, but would like to. I just had
traditional blood tests, and a low cortisol level was enough proof to
get an endocrinologist to run the ACTH stimulation test which has
confirmed the diagnosis of Addison's disease/adrenal insufficiency. I
am now on hydrocortisone (cortef) to replace what my body does not produce.


And since my ACTH is abnormally low, they are know looking into it being
a secondary cause, a pituitary problem. (The secondary cause of thyroid
conditions is also a pituitary cause, hypopituitarism - answering what
you mentioned above).


> and since Dr. Skinner won't treat
> adrenal fatigue, how can i best get this treated? Approach my GP? try some
> supplements? If supplements, which ones? Which books should I get? I'm
> looking for books this year for myself for Christmas, so which ones help
> hypoglycaemia/hypothyroidism? I think some of the Barnes books would help
> but the hpyoglycaemia one is out of print in the UK and the hypothyroidism
> one takes weeks to order from amazon.co.uk.
> I've just been offered a new job, closer to home, but it requires walking
> through Brum city centre, which will take about 20 minutes a day each way.
> As is, if i tried to do that, I'd collapse as soon as I got there, if not
> sooner, because of shaking, trembling and etc. Notice periods at this job
> are a month, so I can't take up the post for a month from now, so basically
> I've got a month to get my stuff sorted.
> The sugar is waking me up at 4am now, keeping me awake the rest of the
> night, because of the shaking, hungry, and anger at not being able to sleep.
> I'm spending all my days dead tired and ready to fall over at any time, yet,
> when i get home, around 7pm, i wake up, and i'm bouncing around all evening.
> Yet at 11, i fall over asleep, comatose, but i'm up again at 4, hyper, angry
> about not sleeping, knowing I have to work the next day, etc.
> Any thoughts, anyone?
> (Except watchman, no iron stuff please, I'm not interested.)
> Jen
You really need your doctor to look into seeing if you have adrenal
insufficiency since it can be quite serious.


In the reference section of this article that was posted here previously,


mentioned is something about reversible hypothyroidism...
one specifically glucocorticoid-reversible hypothyroidism...

Gharib H, Hodgson SF, Gastineau CF, Scholz DA,
Smith LA. Reversible hypothyroidism in Addison's
disease. Lancet 1972; ii: 734-736.

Clin Endocrinol Metab 1985 Nov;14(4):947-76


Adrenocortical insufficiency. Burke CW.

"In addition, cortisol deficiency has secondary
endocrine effects, e.g. glucocorticoid-reversible

Since levoxyl makes me feel like crap and just increases my need for
cortef, I'm hoping that this could be the case -
glucocorticoid-reversible hypothyroidism... I'm not sure if the
articles have out of date information (1972 & 1985) or not, haven't
looked up the articles.

Anybody else heard of glucocorticoid reversible hypothyroidism??? My
current endo says no... but I don't exactly think he's too on the ball.

So, maybe my hypothyroidism *is* reversible... if I just didn't have
such a highly elevated TPO antibody. Even though it has dropped from
1099 to 573, although the lab reference says less than 2 is normal...
But maybe they can drop completely...

So, how do antibodies drop??? It can't just be because of having
thyroid hormone in the blood stream, I have what is considered *normal*
levels of T4 in my blood stream and after
starting/stopping/starting/stopping/starting the medication, my T4 has
fluctuated only slightly. So what does happen? Could it be the effects
of the cortef that has brought down the antibodies? I *think* this may
be what happens: When other people who experience the antibodies going
down once on thyroid meds, that it is because the thyroid meds increase
cortisol metabolism, so that it is effect of cortisol, not that it is a
direct effect of the thyroid hormone. Just sets off a reaction in the
chain. Again, this is just MO of how it may work, not that I have read
this, just coming from my understanding of the process. What I have
read is that thyroid meds increase cortisol metabolism (which is why
someone who is hypocortisolemic can go into an adrenal crisis when
thyroid meds are initiated) and that being placed on thyroid hormones
can reduce thyroid autoantibodies. Then since glucocorticoids have
immunosuppressive effects, my hypothesis makes sense to me.

Anybody know... deT???





Adrenal Steroids

The adrenal cortex is a factory for steroid hormones. In total, at least two to three dozen different steroids are synthesized and secreted from this tissue, but two classes are of particular importance:

Class of Steroid Major Representative Physiologic Effects
Na+, K+ and water homeostasis
Glucose homeostasis and many others

Additionally, the adrenal cortex produces some sex steroids, particularly androgens, a talent of considerable importance in such diseases as congenital adrenal hyperplasia.

Like all steroids, adrenal "corticosteroids" are synthesized from cholesterol through a series of enzyme-mediated transformations. The details of these pathways are presented elsewhere, but the major branches are easy to understand.

Each of the three major pathways involves sequential processing by a group of enzymes, some of which reside in endoplasmic reticulum and others inside mitochondria. Hence, synthesis involves shuttling of the steroids between these two organelles.

Synthesis of the different steroids is not uniformly distributed through the cortex. For example, the outermost group of cells (zona glomerulosa) synthesizes aldosterone, but essentially no cortisol or androgens because those cells do not express the enzyme 17-alpha-hydroxylase which is necessary for synthesis of 17-hydroxypregnenolone and 17-hydroxyprogesterone. That enzyme is however present in cells of the inner zones of the cortex (zonae fasiculata and reticularis), which are the major sites of cortisol production.

Like all steroid hormones, cortisol and aldosterone bind to their respective receptors, and the resulting hormone-receptor complexes bind to a hormone response element to modulate transcription of responsive genes. Although the physiologic effects of these two steroid hormones are distinctly different, their receptors are quite similar and, most interestingly, they bind to the same consensus response element in DNA! How then is it possible to get hormone-specific responses? Follow the path to the next topic to find out at least part of the answer.