Googling around, nothing jumps out at me - that is, I see opinions on
both sides of the issue, with "no relation" probably being the most
common.

Thanx.

You should go to cushings.invisionzone.com and click on the podcasts of
interviews with my endo, Ted Friedman.  In them, he discusses the
distinctions between central hypothyroidism vs. secondary.  TSH is a
pituitary hormone, btw, so there's that pesky HPA axis again.   ;-)

Elevated thyroid lowers cortisol, and elevated cortisol counteracts
thyroid.

Susan

  Med Hypotheses. 2004;62(3):431-7. Links
Anti-thyroid thioureylenes in the treatment of psoriasis.

Elias AN.
Division of Endocrinology, Department of Medicine, Diabetes &
Metabolism, University of California, Irvine UCI Medical Center, 101
City Drive South, Bldg. 53, Rm. 218C, Orange, CA 92868, USA. anel...@uci.edu
Psoriasis is a common skin disorder associated with significant
morbidity. Many agents are used in the medical management of this
debilitating condition with the newer anti-cytokine agents being the
most recent addition to the pharmacological armamentarium to battle the
disorder. Cost concerns are very important with the newer "biologic"
treatments costing in excess of 10,000 US dollars annually. The need for
cheaper, orally administered agents is therefore imperative. This paper
addresses the potential role of anti-thyroid thioureylenes,
propylthiouracil and methimazole, in the treatment of psoriasis and
reviews the possible mechanism of action of these drugs in this
disorder. It is hypothesized that the beneficial effect of anti-thyroid
thioureylenes in psoriasis is linked to their effect as
anti-proliferative agents as reflected by significant decrease in
markers of cellular proliferation such as proliferative cell nuclear
antigen in biopsy specimens after treatment with these drugs.
Propylthiouracil has been shown to bind to the hepatic T 3 receptor and
it is possible that propylthiouracil (6-n-propyl-2-thiouracil) binding
to the ligand-binding site normally occupied by T 3 impairs
transcription by inactivating the effect of T 3 as well as by squelching
retinoic X receptor heterodimer formation with other receptors of the
steroid receptor superfamily such as the peroxisome
proliferator-activated receptor, retinoic acid receptor and vitamin D
receptors.
PMID: 14975517 [PubMed - indexed for MEDLINE]

BMC Dermatol. 2004 Apr 30;4:4.  Links
Serum TNF-alpha in psoriasis after treatment with propylthiouracil, an
antithyroid thioureylene.

Would hypo-thyroidism then be a good thing - and would taking thyroid
hormones to treat hypo-thyroidism possibly be a bad thing?

--

Or, are you saying that elevated cortisol suppresses thyroid, and
therefore reducing cortisol would improve both thyroid and psoriasis?

--

And of course, the answer may well be, "it depends".

I would never give it to you. You need a shrink, way outside my
permit.

I am not ignoring the ACTH, the ACTH is involved in signalling the
adrenals to produce hormones, the ACTH shuts down when the cortisol
gets to a certain level. The ENTIRE cascade from the Hippothalmus , to
the pituitary to the adrenals gets shut down by the cortisol feeback.

You are strange, you have no problem taking a foreign chemical like
Antalarmin, never found in your body naturally, but you wont think of
taking a natural cortisone. Very strange. If you have a chemical
adrenalectomy(or the equivalent) you can kill yourself if you have
resistance or bound cortisol. IT IS VERY DANGEROUS, see plechner, he
has a whole section on High Cortisol.

You DO need thyroid hormones if you take long acting cortisone, since
without thyroid hormones the cortisone may still be active when you
takethe next dose and you risk piling dose upon dose, and that is when
you can get problems. Thyroid metabolises cortisol. Read Plechner he
has 40 years of experience as a clinician, more than you I suspect.

I know my own body. Get to know yours, we are all different. Saliva
tests are very useful  eg :

If you are cortisol RESISTANT the saliva test is useful. If you have
HIGH cortisol on the saliva test AND your eosinophil count is high and/
or your lymphocytes are high ie you have inflammation, then the
cortisol is likely inactive, and probably due to cortisol RESISTANCE.
The cortisol receptors are resistant to the action of cortisol and so
the signal back to the adrenals to switch off does not get received
and the adrenals keep pumping the stuff out.

If you can control cortisol resistance without taking cortisol then
you are fortunate. Vitamin D can sensitize the receptors and may
explain its function in psoriasis, but it wont solve the resistance
problem adequately, for if it did, I suspect the psoriasis story would
be history already. PPARs may also be useful.

If you have LOW cortisol on the saliva test then you need extra
cortisol, and good luck getting that without taking cortisol.

I would only get a serum cortisol test if the saliva test showed
normal. (I have done the serum test and that was also high).  If the
saliva test is abnormal(low/high) then the treatment is to take
cortisone,or embark on an endless alternative therapy pathway which
may or may not work and may take decades. I dont have that time.

Why is it acceptable for a diabetic to take insulin, a hormone that
will kill you stone dead if you take too much, but it is not
acceptable to take the  hormone that without which you will also die,
cortisol ? If your cortisol is high and you are resistant , then it is
as good as having almost none, and it is sensible to make up the
difference. If your cortisol is low then you also need to make up the
difference.

HOW MAY MY HEALTHCARE PROFESSIONAL, DETERMINE IF THE HIGH CORTISOL
VALUE, IS ACTIVE OR BOUND?

By Alfred J. Plechner, D.V.M.

When there is an over production of cortisol, this is called Cushing
syndrome. But the real Cushing syndrome is an excess production of
active cortisol, produced by the middle layer of the adrenal cortex.
Dr. Harvey Cushing identified a tumor in the pituitary gland that
produced a hormone called ACTH, which caused the middle layer adrenal
cortex to produce too much active cortisol. It is thought that a tumor
of this middle layer, adrenal cortex, may also cause the production of
too much active cortisol. It is also thought that giving too much
cortisone can cause an increased production of active cortisone which
is true, if the cells in the middle adrenal cortex are still
productive, or this cannot happen. If these cells are still
productive, and exogenous steroids are, this is referred to as
iatrogenic, which means that the use of a cortisol replacement by your
healthcare professional has caused this excess production of active
cortisol. It is also thought that, providing cortisone to a patient,
may lead to an inflammation of the pancreas, including the possibility
of diabetes. This has been proven wrong. The general belief, now, with
the educated healthcare professionals, is that the disease causes the
pancreatic problems. It is not the cortisone replacement.

How do you know that an elevated amount of cortisol is active or
inactive? An elevated, empirical, amount of cortisol, does not
guarantee that it will work in that patient. You may be told that the
cortisol level is elevated, so it may be important to give the patient
a chemical to reduce the amount of cortisol that is being produced
from the middle layer adrenal cortex. These levels may be empirical,
and can only be proven viable, by looking at those levels, that active
cortisol regulates. If these levels of high cortisol are bound or
defective, the chemical, given to reduce these high, but defective
levels, may really hurt the patient. Because my findings have not been
accepted, do not mean they do not exist.

Empirical levels of cortisol will never be the answer to helping the
patient. Even if your healthcare specialists do not relate to this,
they can relate to the fact, that doing a complete blood count called
a CBC, may show a deficiency in two types of white blood cells. Those
deficiencies include a reduced number of lymphocytes and eosinophils.
If these cells are present in normal numbers, this may be an inactive
cortisol. If these cells, are in a reduced state, the elevated volume
of cortisol is probably active, and the use of chemical intervention
may be indicated and of value. If this chemical is used in a patient
that has high, inactive, cortisol, could cause that patient to lose
their life.

It sounds like it is time, to do comparative levels, before the
chemical treatment is prescribed. By including total estrogen with
Plechner's Syndrome, this will give you much better insight as to
whether the cortisol is active or inactive. If the total estrogen is
high, then the cortisol is inactive. If the total estrogen is low, as
well as the IgA, IgM and IgG, the high cortisol is active, and may be
a true Cushing Syndrome. To do a cortisol stimulation test, if the
cortisol is inactive, may be of little value in diagnosing while
trying to diagnose this disorder.

Because the laboratory indicates that there is an over abundance of
cortisol, does not mean the laboratory test is accurate. Also, are you
seeing actual signs of an increased, active cortisol?

What are the signs you might expect to see, with an active excess of
cortisol? You should see increased consumption of water and increased
urination. There should be hair loss without inflammation and pruritis
[itchiness]. Even though there may be calcification of the skin, this
also occurs in other disorders besides with a high level, defective or
bound cortisol. This can also occur with kidney disease, diabetes,
irritable bowel syndrome, an IgA deficiency, a digestive enzyme
deficiency, chronic intestinal parasites and a food, too high in oil
based foods. Let's go from here.

Please check out, all, the above first, and if any of the above
clinical syndromes are not involved, it is time to check to see if the
high cortisol is really real. I have already indicated ways to
determine this, but are there other things that can cause an elevated
cortisol result which may be defective?

First of all, you need to guarantee, that the serum sample is spun
down, and refrigerated immediately. The use of a temperature strip may
be the thing of the future, to make sure the sample arrives
refrigerated. The laboratory needs to also keep all these samples
refrigerated. It is common practice at many laboratories to leave
samples out, and to run them in batches. If this is done, all the
cortisols plus other hormones and antibodies may be abnormally high.
Again, this may lead to the use of a chemical, to reduce the elevated
cortisol, which only occurred, because the serum was improperly
handled, and reached room temperature or higher.

Why not use Plechner's Syndrome and receive the results that are
comparative and not empirical?

If the blood sample is to be handled correctly, you need to send the
sample to qualified laboratories, because many of these laboratories
have neither the staff nor equipment to guarantee you and your
healthcare professional accurate results. Improper handling of the
blood plus inaccurate results, could lead to a catastrophe for either
you or your pet. But if you are not sure of this laboratory, there is
a laboratory listed on my home page that is qualified.

It is very important to realize, that even though there may be a large
amount of inactive cortisol present, its presence may still cause
clinical side effects. This is important to know, because, if active
cortisol is given, a lower dose of the exogenous cortisol might be
used, to reduce the possibilities of increased water consumption and
increased urination.

If the IgA level is below 60, in you or your pet, administration of an
active cortisol will not be absorbed and the problem will continue.
Please do not accept any cortisol level, without considering the
possibilities, this might lead to an inaccurate result that could
cause you or your pet fatal damage.

Recent evidence from prominent schools of veterinary medicine,
indicate that elevated levels of estrogen can mimic high, active
cortisol. What kind of cortisol replacement will be efficient for you
and your pet or pets?

If you have tried homeopathic, holistic and herbal replacement, with
little to no response, you must realize this layer, of the adrenal
gland, may be permanently damaged, and not merely fatigued. You need
to realize, that you cannot enhance the integrity of tissue that is
permanently damaged. To give to you or your pet embryonic or adult
remnants of the organs that produce these hormones is naive. These
remnants are digested by the enzymes that are present, and only enter
the blood stream as proteins and amino acids, and not hormones!
Western synthetics may be your only hope but in the early phases, only
through injections and not oral supplementation.

It is thought by the medical profession, that on the water retention
scale, Hydrocortisone is a 2, which is the highest, and Prednisolone
is a 1. However Prednisone is preferred by most medical doctors.
Interestingly enough, the doctors are afraid that a cortisone
supplement may cause liver damage, yet they still use Prednisone,
which needs to be converted in the liver, to Prednisolone! Why? The
use of Medrol in dogs and in humans may provide the least water
retention. Cats usually do very well on Prednisolone. Horses seem to
do best on thyroid hormone, because their cortisol imbalances are
often due to adrenal suppression that may be temporary or due to the
use of feed with elevated levels of estrogen present. Different hays,
throughout the country may be to blame. I do not believe this is
recognized just yet.

The importance of this article is to be aware, and not fall into those
tragedies that have occurred do to inaccurate laboratory results and
an absence of realizing the difference between active and inactive
cortisols.

Other hormones that occur in the body may also fall into this
category. This is why salivary and 24 hour urine tests have been
developed. These tests may distinguish between free and bound
hormones, but what is the guarantee, that the receptor sights, for the
use of these active hormones, are not blocked? There are no
guarantees!

You must observe the clinical signs and symptoms of your patient, and
decide the best way to heal that patient and not your wallet!

Why are you trying to sensitize your cortisol receptors , when you
dont have cortisol resistance, for if you had you would have HIGH
cortisol readings on saliva and serum tests ? The standard treatment
for cortisol resistance is adding enough cortisone to overcome the
resistance and switch off the HPA feedback. See here :

Therapy of Glucocorticoid Resistance syndrome
http://www.endotext.org/adrenal/adrenal16/ch01s04.html

You say that you have low active cortisol and probably bound, so you
need to add active cortisol. Why are you trying to stop CRH ? Makes no
sense. You probably have a form of Addison's, but certainly you dont
have resistance. I don't know how you can overcome a shortage of
ACTIVE cortisol without adding it.

See here :

New Discovery?: High Cortisol Binding Globulin as cause of Addison's?

"hypercortisolemia(high cortisol) which often causes symptoms of
adrenal insufficiency(weakness)."

How ? If the cortisol is inactive or you are resistant there is no
feedback and the adrenals keep pumping out hormones, so how does that
give symptoms of adrenal weakness ? There is a disease called CAH
where this happens and they have to take oral cortisone to shut down
the feedback loop and stop the adrenal hormone production.

When you say you also have low cortisol and you want to stop the CRH
producing ACTH, if you are having a low cortisol episode, and you
lower it even further by stopping the CRH, you will probably go into
an Addison's crisis.

I dont follow your logic.

Thrash around in the dark at your leisure.

Enough.