rT3 high, how to deal with it, #2

[JanSz]

Threre is at least two men with high RT3

The only treatment that I was able to google is:
Medical Treatment of Wilson's Temperature Syndrome (WT3 protocol)
http://www.wtsmed.com/Medical.htm

I think chilln makes a good point,

Dr Crisler
please chime in and educate us.
==============================================
This is second aproach at this topic.
first one was here:
http://musclechatroom.com/forum/showthread.php?t=924&highlight=rT3+high%2C+deal


http://musclechatroom.com/forum/showpost.php?p=30772&postcount=38

JanSz - after Dr Crisler's unfavorable review of the U-opioid antagonists, I'm not sure Dr Crisler is necessarily going to agree with this thyroid reset mechanism.

I suggest you propose this as a discussion item, via a separate thread. Then if Dr Crisler chimes in and suggests it's interesting, then perhaps suggest it as something a forum member might want to consider (along with their medical professional adviser of course).

http://musclechatroom.com/forum/showpost.php?p=30716&postcount=32



TSH 2.074 uIU/mL [0.450-4.500]
T4 Free 1.10 ng/dL [0.61-1.76]
T3 Free 3.1 pg/mL [2.3-4.2]
Reverse T3 281 pg/mL [90-350]


http://musclechatroom.com/forum/showpost.php?p=30742&postcount=36

RT3 has come down... was 350 last time.

================================================== =====================

http://musclechatroom.com/forum/showpost.php?p=31017&postcount=9

T3 Reverse 42 (11-32 ng/dl)
FT4 1.2 (.8-1.8)
FT3 321 (230-420)
TSH 2.31 (.40-4.50

[hardasnails1973]

Cortisol/dhea imbalances
starvation
selenium, zinc, iodine, potassium defieincy
copper imbalances

[JanSz]

Cortisol/dhea imbalances
starvation
selenium, zinc, iodine, potassium defieincy
copper imbalances

Thank you, I know I could always count on you.
Lets wait and see if dr John have a time to explain to us how it is really done.

I will bump this thread from time to time while waiting.

This thread is specifically about high RT3, specifically waiting for dr John's opinion.
Thank you.

[JanSz]

Notes of:

Ron Rothenberg MD
Clinical Professor
Preventive and Family Medicine
UCSD School of Medicine
Founder, California Healthspan Institute
www.eHealthSpan.com
(800) 943-3331

http://www.ehealthspan.com/download/
===========================================

Notes on thyroid:
http://www.ehealthspan.com/download/4-Thyroid1.1.doc

On the bottom of presentation discussed:
Wilson’s reverse T3 dominance syndrome
and
Treatment – Wilson’s syndrome

Sunday, October 28, 2007 2:38 PM 46477 4-Thyroid1.1.doc

Natural Thyroid Replacement Therapy
In an Anti-Aging Practice
New Thyroid Concepts
============================================

Low T3 , high RT3 predicts mortality
• Surviving patients improved the T3/RT3 ratio

[wondering]

work on D1 enzyme and RT3 will take care of itself. no?

[chilln]

work on D1 enzyme and RT3 will take care of itself. no?

Unlikely, because deiodinase D1 doesn't act specifically to boost any one of the thyroid hormone fractions.

Ie: deiodinase D1 simply boosts several thyroid hormone conversions:

..T4 -> T3
..T4 -> rT3
..T3 -> 3,3T2
rT3 -> 3,3T2

(diagram here)
http://en.wikipedia.org/wiki/File:Iodothyronine_deiodinase.png

[Investmentbanker]

How would one "work on" the D1 enzyme? I have a FT4 -> FT3 conversion problem but when put on Armour, even at 30 mg, was very shaky, anxious, etc. Stopped taking it. Still very low on FT3 but feel okay, a little sluggish but okay. I am hoping getting my SHBG down will help with energy and libido.



Unlikely, because deiodinase D1 doesn't act specifically to boost any one of the thyroid hormone fractions.

Ie: deiodinase D1 simply boosts several thyroid hormone conversions:

..T4 -> T3
..T4 -> rT3
..T3 -> 3,3T2
rT3 -> 3,3T2

(diagram here)
http://en.wikipedia.org/wiki/File:Iodothyronine_deiodinase.png

[hardasnails1973]

Examine a person's lifestyle, nutritional status and imbalances, identify metabolic roadblocks, cortisol/dhea imbalance, other hormonal imbalances.
i can not emphasis this enough !!

[JanSz]

To my list of tests, on post #44
http://anabolicminds.com/forum/male-anti-aging/66268-jans-bloodtest-april13-2.html

I have added:

27 ------------ T3, Total (859X)
28 ------------ T4, Total (Thyroxine)
================================================== =======

so Wilson’s syndrome
• Ratio of T3/RT3 < 10:1

could be loked at and evaluated.
-------------------------------------------------------------------------
http://www.ehealthspan.com/download/4-Thyroid1.1.doc
RT3 and cellular metabolism

• RT3 decreases cellular energy production
• T3 reverses this decline


• Okamoto R et al. Adverse effects of reverse triiodothyronine on cellular metabolism as assessed by 1H and 31P NMR spectroscopy. Res Exp Med (Berl) 1997;197(4):211-7
Low T3 , high RT3 predicts mortality
• Surviving patients improved the T3/RT3 ratio
• Sick euthyroid syndrome

• Schulte C et al. Low T3-syndrome and nutritional status as prognostic factors in patients undergoing bone marrow transplantation.
Bone Marrow Transplant 1998 Dec;22(12):1171-8
Thyroid and Ankylosing Spondylitis
• FT4, FT3 and TT3 were significantly lower
• TSH and TT4 were found to be in the normal range
• rT3 was significantly increased.
• The prevalence of anti-thyroid antibodies was significantly higher in the AS-group.


• Lange U et al. Thyroid disorders in female patients with ankylosing spondylitis.
Eur J Med Res 1999 Nov 22;4(11):468-74


Selenium supplementation and thyroid
• Critically ill patients
• 500 mcg Seleneium, 150 mg alpha tocopherol, 13 mg zinc
• Normalization of TT3. TT4 and RT3 with improvement in T3/RT3 ratio with selenium
• No chance with alpha tocopherol or zinc (JanSz note, I think dr ment change not chance)

• Berger MM et al. Influence of selenium supplements on the post-traumatic alterations of the thyroid axis: a placebo-controlled trial. Intensive Care Med 2001 Jan;27(1):91-100
Thyroid and regaining lost weight after dieting
• T3/RT3 falls during acute and chronic calorie restriction
• Is this a factor why lost weight is usually regained?

• Weinsier RL et al. Do adaptive changes in metabolic rate favor weight regain in weight-reduced individuals? An examination of the set-point theory. Am J Clin Nutr 2000 Nov;72(5):1088-94
Anti-Aging Medicine
Thyroid replacement therapy
Wilson’s reverse T3 dominance syndrome
• Stress….Increased Cortisol….Impaired T4 to T3 conversion….increased RT3 conversion
• RT3 occupies binding sites of T3, impairs T4 to T3 conversion and may feed back to decrease TSH
• “Hypometabolism” produced which decreases enzyme activity in all systems…
• Fatigue, headache, migraine, PMS, irritability, fluid retention, anxiety and panic attacks, hair loss, depression, decreased memory and concentration, low sex drive, unhealthy nails, low motivation and ambition
• No references to Wilson’s syndrome on medline
Wilson’s syndrome• Ratio of T3/RT3 < 10:1
• Low body temp
• Symptoms
Treatment – Wilson’s syndrome
• Compounded extended release T3 7.5 mcg q12 hours x 2 days
• If oral temp not 98.2 increase to 15 mcg q 12 hours x 2 days
• Increase till 98.2 or symptoms of thyroid excess
• Then taper back at same rate
• Then temp should stay normal or another cycle required

[wondering]

Iodoral and selenium are helpful. Iodoral made a big difference in me in just a matter of days.

worth looking into.


How would one "work on" the D1 enzyme? I have a FT4 -> FT3 conversion problem but when put on Armour, even at 30 mg, was very shaky, anxious, etc. Stopped taking it. Still very low on FT3 but feel okay, a little sluggish but okay. I am hoping getting my SHBG down will help with energy and libido.

[Investmentbanker]

when you say a big difference, what did you mean...energy, libido, etc??


Iodoral and selenium are helpful. Iodoral made a big difference in me in just a matter of days.

worth looking into.

[wondering]

little bit more energy, much improved clear-headedness (is that a word ?)


when you say a big difference, what did you mean...energy, libido, etc??

[JanSz]

For $20 I can buy this presentation.
Most likely it is very much related to dr Ron Rothenberg's notes I posted link to, above.

Looks like dr Rothenberg believe in Wilson’s syndrome
and how to treat it.
The thing is, we are on dr John's board
waiting for his blessing or other details.
Dr John, rules.
================================================== ========
Less than 2 months ago.

http://www.prolibraries.com/a4m/?select=session&sessionID=1801
PC07b - Thyroid Replacement Therapy
$20.00 Purchase Conference: A4M Las Vegas 2008
Speaker: Ronald Rothenberg, MD
Date/Time: December 11, 2008 8:45 am - 9:30 am
Length: 30m 54s - 68 Slides

================================================== ========
http://www.prolibraries.com/a4m/?select=session&sessionID=1524
PC04c - Thyroid Hormone
$20.00 Purchase Conference: A4M Washington DC 2008
Speaker: Ron Rothenberg, MD
Date/Time: July 17, 2008 9:20 am - 10:00 am
Length: 40m 09s - 98 Slides
================================================== ========

http://www.prolibraries.com/a4m/?select=session&sessionID=1309
PC01c - Thyroid Hormone Deficiency - Diagnostic and Treatment T3, T4, THS
$20.00 Purchase Conference: A4M Orlando 2008
Speaker: Ron Rothenberg, M.D.
Date/Time: April 25, 2008 12:00 am - 12:00 am
Length: 46m 44s - 97 Slides
================================================== ========

[chilln]

Examine a person's lifestyle, nutritional status and imbalances, identify metabolic roadblocks, cortisol/dhea imbalance, other hormonal imbalances.
i can not emphasis this enough !!


You aren't emphasizing this enough! They're not getting the message :biggrin:

[JanSz]

:
Originally Posted by hardasnails1973
Examine a person's lifestyle, nutritional status and imbalances, identify metabolic roadblocks, cortisol/dhea imbalance, other hormonal imbalances.
i can not emphasis this enough !!



You aren't emphasizing this enough! They're not getting the message :biggrin:

Please do not take this thread off track.
This thread is about high RT3.
When RT3 is sufficiently high, others call it
Wilson’s reverse T3 dominance syndrome.

I have open #2 thread because the first one was side-tracked.

Please open new thread and we will discuss other aspects of thyroid treatments, worthy topic.

When discussing (on this thread) please assume that the (good) points raised by HAN are already accounted for by treating provider and RT3 is still very high.
.
.

[JanSz]

Some of BigPharma links;

Merck Manual
Euthyroid Sick Syndrome
http://www.merck.com/mmpe/sec12/ch152/ch152c.html
http://www.merck.com/mmpe/sec12/ch152/ch152c.html?qt=Euthyroid%20Sick%20Syndrome&alt=sh

Treatment

Treatment with thyroid hormone replacement is not appropriate. When the underlying disorder is treated, results of thyroid tests normalize.

This is CLEAR BIG-PHARMAs response.
You just go ahead and try to find the "underlying disorder", good f**ken luck.
------------------------------------------------------------

emedicine.medscape
Euthyroid Sick Syndrome

The effects of nonthyroidal illness
Triiodothyronine and reverse triiodothyronine

http://emedicine.medscape.com/article/118651-overview
------------
Euthyroid Sick Syndrome: Multimedia
http://emedicine.medscape.com/article/118651-media

Conditions that affect thyroid function tests
Laboratory Studies
http://emedicine.medscape.com/article/118651-diagnosis

-----------------------
http://emedicine.medscape.com/article/118651-treatment
Medical Care
There is no prospective study to date demonstrating benefit or harm of thyroid hormone replacement in NTI. Thyroid hormones have been used in the setting of NTI in various settings with T4 and T3 replacement and still remain controversial. Dr De Groot has supported the notion that nonthyroidal illness syndrome is a manifestation of hypothalamic-pituitary dysfunction, and in view of current evidence, he proposed that treatment should be considered with appropriate replacement therapies such as pituitary hormones, hypothalamic factors in addition to thyroid hormones.

[chilln]

bump - just hoping more people chime in on this thread. It's very promising.

[chilln]

Finally.

I think I've found the best solution - and this guy is a medical professional - a pharmacist - in Australia (of all places)

http://www.custommedicine.com.au/blog/2007/04/17/reverse-t3-dominance/

Hiis conlcusion (bottom of page) is:

"We have found that by using a consistent low dose of T3 over two to three months without the need of cycling the dose, as described by Dr Wilson, in addition to addressing the causes of improper T4 metabolism, many patients have responded favorably with improved symptoms and a reduction in reverse T3 levels."

The statement about addressing the causes of improper T4 metabolism is mentioned a little further up the document, ie:

"In addition nutrients such as selenium, zinc, Vit B6, B12 and E, iron and iodine should be supplemented as they are necessary cofactors for the proper conversion of T4 into T3."

I think this gent has the solution.

[JanSz]

Finally.

I think I've found the best solution - and this guy is a medical professional - a pharmacist - in Australia (of all places)

http://www.custommedicine.com.au/blog/2007/04/17/reverse-t3-dominance/

Hiis conlcusion (bottom of page) is:

"We have found that by using a consistent low dose of T3 over two to three months without the need of cycling the dose, as described by Dr Wilson, in addition to addressing the causes of improper T4 metabolism, many patients have responded favorably with improved symptoms and a reduction in reverse T3 levels."

The statement about addressing the causes of improper T4 metabolism is mentioned a little further up the document, ie:

"In addition nutrients such as selenium, zinc, Vit B6, B12 and E, iron and iodine should be supplemented as they are necessary cofactors for the proper conversion of T4 into T3."

I think this gent has the solution.

One down, so many to go.

In vicinity of the 2-3 months period, when planning to start tappering back, it would be good to know the desirable levels of important thyroid analytes, so one is able to make sure that he reached planned end point of theraphy.
================================================== ==================

I am not confortable with
http://www.custommedicine.com.au/blog/2007/04/17/reverse-t3-dominance/
explanation of ratio, namely this:
"Ideally the ratio of T3/rT3 multiplied by 100 should be between 1.06 to 1.13. "
Working with any numbers requires careful watching units.
Better example would help.
Those numbers would not work if we use results from Quest Diagnostics.
Untill we know the units used above we cannot use their condition to figure out RT3 dominance
-----
But using Quest Diagnostics units would work if we use condition for RT3 dominance as done by dr Rothenberg (post #4 & #9 this thread)
hes wrote the condition as:

Wilson’s syndrome
• Ratio of T3/RT3 < 10:1
----------------------
Quest Diagnostics reports like this:

T3,Total (60-181) ng/dL
T3, Reverse (11-32) ng/dL
--------------------

at lower range the ratio is
60/11~6
at higer range the ratio is
181/32~6

someone with RT3 at high range RT3~32
and T3 at low range T3~60
would have this analytes within normal range, but

would have ratio 60/32~2 less than 10, and would have Wilson's syndrome

Basically dr Rothenberg is saying that we need to have 10x or more of T3 relative to RT3 to avoid RT3 dominance.
.
================================================== =================

("Wilson's Syndrome" - also known as Multiple Enzyme Dysfunction or MED)

[JanSz]

http://journals.indexcopernicus.com/abstracted.php?icid=250423


Serum rT3 and T3/rT3 are prognostic markers in critically ill patients andare associated with post-mortem tissue deiodinase activities.
------------

Conclusion: In critically ill patients who required more than five days intensive care, rT3 and T3/rT3 were already prognostic for survival on d1. On d5, T4, T3, but also TSH levels are higher in patients who will survive. SerumrT3 and T3/rT3 were correlated with post-mortem tissue deiodinase activities.

[Dr. John Crisler]

Cortisol/dhea imbalances
starvation
selenium, zinc, iodine, potassium defieincy
copper imbalances
Yes, ALWAYS look to nutritional deficiencies.

[Dr. John Crisler]

work on D1 enzyme and RT3 will take care of itself. no?
Yes!

[Dr. John Crisler]

Unlikely, because deiodinase D1 doesn't act specifically to boost any one of the thyroid hormone fractions.

Ie: deiodinase D1 simply boosts several thyroid hormone conversions:

..T4 -> T3
..T4 -> rT3
..T3 -> 3,3T2
rT3 -> 3,3T2

(diagram here)
http://en.wikipedia.org/wiki/File:Iodothyronine_deiodinase.png

That is incorrect. D1 is good. D3 is what converts T4->T3, also T3->T2

[Dr. John Crisler]

If people are truly getting results with this program, that is certainly proof of its validity. At least for a portion of the patient population--it sure seems like there is a lot of "it wasn't done right" going on; but granted, this hormonal stuff can be VERY challenging.

These points of science remain:

rT3 has a very short half-life, about 3 hrs. Therefore it does not "build-up" in tissue, or need "clearing".

Supplementing pure T3 (even appropriately as sustained release preparation) does nothing for increasing enzyme D1 activity-and this is the whole problem. D3 is dominating over D1, and so rT3 is being produced antagonistically over T3. Precisely, it's the T4 run through D1 to become T3 that makes the difference. Supplemented T3 does not do this. Picking up D1 acitivity, specifically D1/D3, that is the cure.

I simply have not seen Armour Thyroid increase rT3 as this protocol directly states. And I monitor same. But perhaps it's the other things I am concurrently doing in these patients that is making the difference.

I also do not wish to ramp up heart rate to tachycardic rate as will happen with many by hypersupplementing T3 only.

Again, D1 is the centerpiece of thyroid optiminization.

[Dr. John Crisler]

Iodoral and selenium are helpful. Iodoral made a big difference in me in just a matter of days.

worth looking into.Yes, iodine seems to help a lot in stabilizing thyroid levels in some.

[Dr. John Crisler]

Finally.

I think I've found the best solution - and this guy is a medical professional - a pharmacist - in Australia (of all places)

http://www.custommedicine.com.au/blog/2007/04/17/reverse-t3-dominance/

Hiis conlcusion (bottom of page) is:

"We have found that by using a consistent low dose of T3 over two to three months without the need of cycling the dose, as described by Dr Wilson, in addition to addressing the causes of improper T4 metabolism, many patients have responded favorably with improved symptoms and a reduction in reverse T3 levels."

The statement about addressing the causes of improper T4 metabolism is mentioned a little further up the document, ie:

"In addition nutrients such as selenium, zinc, Vit B6, B12 and E, iron and iodine should be supplemented as they are necessary cofactors for the proper conversion of T4 into T3."
I think this gent has the solution.
I think this is where the answer actually lies.

D1!

BTW, a LOT of good medicine comes out of Australia.

[JanSz]

If people are truly getting results with this program, that is certainly proof of its validity. At least for a portion of the patient population--it sure seems like there is a lot of "it wasn't done right" going on; but granted, this hormonal stuff can be VERY challenging.

These points of science remain:

rT3 has a very short half-life, about 3 hrs. Therefore it does not "build-up" in tissue, or need "clearing".

Supplementing pure T3 (even appropriately as sustained release preparation) does nothing for increasing enzyme D1 activity-and this is the whole problem. D3 is dominating over D1, and so rT3 is being produced antagonistically over T3. Precisely, it's the T4 run through D1 to become T3 that makes the difference. Supplemented T3 does not do this. Picking up D1 acitivity, specifically D1/D3, that is the cure.
I simply have not seen Armour Thyroid increase rT3 as this protocol directly states. And I monitor same. But perhaps it's the other things I am concurrently doing in these patients that is making the difference.

I also do not wish to ramp up heart rate to tachycardic rate as will happen with many by hypersupplementing T3 only.

Again, D1 is the centerpiece of thyroid optiminization.

This is a second thread about RT3.
We already have been thru the "usual"
selenium, zinc, Vit B6, B12 and E, iron and iodine supplements.
So lets assume that we have done due diligence in that area.
-------------------
Reason why T3 is supplemented:
existing T3 will reduce TSH, TSH-->0
when TSH~0 then T4 is not produced
after certain time (2-3 months?) T4 is depleted, T4~0


After the theraphy ends new T4 arrives.
Supposedly, when starting a new the enzymes D1 & D3 work at proper (or better) proportions.

It is explained better here:

http://www.wilsonssyndrome.com/WhyIsIt.htm
http://www.wilsonssyndrome.com/Medical.htm
http://www.wilsonssyndrome.com/SiteMap.htm

WTS appears to be due to a bogging down of the thyroid system due to impaired T4 to T3 conversion. This bogging down of the thyroid system appears to be perpetuated by RT3 in the tissues, as well as perhaps other factors. Once the system is bogged down, it appears that backlogged raw thyroid hormone (T4) can also adversely compete with the active thyroid hormone (T3). Even though T4 is the source of T3, if it's not being converted well it can actually be a significant hindrance!

Wilson's T3 protocol is aimed at depleting RT3 levels in the tissues of the body, for a time. This is accomplished by reducing T4, its only source. T4 is reduced by reducing TSH (Thyroid Stimulating Hormone). TSH is reduced by giving patients pure T3 directly.

When patients are given pure T3 directly, their bodies sense that they are getting enough thyroid stimulation so they reduce their own production of thyroid hormones.

The purpose of the treatment is not so much to give patients' thyroid glands a rest (although that does happen), as it is to clear RT3 (by clearing T4) out of the tissues so that their thyroid systems can get de-bogged, cleaned out, and reset. This appears to be what enables the patients' thyroid systems to function well on their own again. Wilson's T3 therapy does not need to be taken for life, rather usually only a few weeks or months.
================================================== ========
=======================
http://www.wilsonssyndrome.com/WhyUndiagnosableWithThyroid.htm

wilsonssyndrome.com/WhyUndiagnosableWithThyroid

Hearing about the importance of T4 to T3 conversion and RT3, some physicians and labs have started looking at Total T3, Free T3, Total T4, Free T4, Total RT3, and T3/RT3 ratios. But none of these tests demonstrate T4 to T3 conversion in the tissues and cells of the body. They only show what's floating around in the blood stream just like any other blood test. Some doctors and labs are starting to tell people that there are new tests unlike the normal thyroid tests that can confirm or deny WTS. But that's not true. Some doctors and labs are saying, in effect, "OK conversion, let's measure T3 and RT3 in the blood." However, presenting and relying on a new line of inconclusive thyroid blood tests that replaces the first would just be putting us right back where we started. This explains why many patients still respond extremely well to the treatment regardless of what any of these tests say. Not only do some of the patients with "normal" tests still respond well, but so do some that are shown as being "abnormal" in a way that's supposedly exactly opposite to WTS. For example, some of the patients with "low" RT3 levels and/or "high" Free T3 levels and/or high T3/RT3 ratios can still respond beautifully well to the WT3 protocol.

[chilln]

Wilson's T3 protocol is aimed at depleting RT3 levels in the tissues of the body, for a time. This is accomplished by reducing T4, its only source. T4 is reduced by reducing TSH (Thyroid Stimulating Hormone). TSH is reduced by giving patients pure T3 directly.

That's not wholly true. Wilson's therapy specifically cycles the dose of T3 from low, to too high and back to low again.

This is a critical aspect of Wilson's therapy. It must not be overlooked.

HOWEVER, if someone chooses to supplement with pure T3 without cycling, in order to achieve the same end result - then that is not Wilson therapy. That is "someone else's therapy".

Let's be very clear about this.

Cycling T3 = Wilson Therapy
Constant dose of T3 = someone else's therapy



When patients are given pure T3 directly, their bodies sense that they are getting enough thyroid stimulation so they reduce their own production of thyroid hormones.

The purpose of the treatment is not so much to give patients' thyroid glands a rest (although that does happen), as it is to clear RT3 (by clearing T4) out of the tissues so that their thyroid systems can get de-bogged, cleaned out, and reset. This appears to be what enables the patients' thyroid systems to function well on their own again. Wilson's T3 therapy does not need to be taken for life, rather usually only a few weeks or months.

Again, this statement completely misses the cyclic part.

Therefore this is not describing Wilson's therapy. This is describing "someone else's therapy".

[JanSz]

That's not wholly true. Wilson's therapy specifically cycles the dose of T3 from low, to too high and back to low again.

This is a critical aspect of Wilson's therapy. It must not be overlooked.

HOWEVER, if someone chooses to supplement with pure T3 without cycling, in order to achieve the same end result - then that is not Wilson therapy. That is "someone else's therapy".

Let's be very clear about this.

Cycling T3 = Wilson Therapy
Constant dose of T3 = someone else's therapy




Again, this statement completely misses the cyclic part.

Therefore this is not describing Wilson's therapy. This is describing "someone else's therapy".

The subject of this thread is how to correct too high RT3.
So any way that works and correct existing problem is fine by me.
=============================

Do you have a place, with link, that describes Wilson's theraphy to your satisfaction? In general, and in specific detail.

I could also use some directions and detailed values to be used for blood testing to monitor progress.
================================================== =======
==============
Same as above for other than Wilson theraphy.

.
.
.

[chilln]

The subject of this thread is how to correct too high RT3.
So any way that works and correct existing problem is fine by me.
=============================

Do you have a place, with link, that describes Wilson's theraphy to your satisfaction? In general, and in specific detail.

I could also use some directions and detailed values to be used for blood testing to monitor progress.
================================================== =======
==============
Same as above for other than Wilson theraphy.

.
.
.

The last page of this document (a link you posted earlier) specifically states the treatment is to ramp up until body temp is too high, then ramp down.

From a health perspective no-one should ramp up their T3 until their body temp is too hot, and then maintain that level of T3 - that's unhealthy. Therefore this is obviously designed to be implemented by ramping up and then immediately ramping down.

http://www.ehealthspan.com/download/4-Thyroid1.1.doc


The Australian pharmacist confirms this point about Wilson's Therapy, in the link I posted earlier, ie:

http://www.custommedicine.com.au/blog/2007/04/17/reverse-t3-dominance/

[Drew]

[QUOTE=chilln;32025]The last page of this document (a link you posted earlier) specifically states the treatment is to ramp up until body temp is too high, then ramp down.QUOTE]

Just for clarification, it doesn't state to ramp up until body temp is too high. What it states is this:

• Compounded extended release T3 7.5 mcg q12 hours x 2 days
• If oral temp not 98.2 increase to 15 mcg q 12 hours x 2 days
• Increase till 98.2 or symptoms of thyroid excess
• Then taper back at same rate
• Then temp should stay normal or another cycle required

http://www.ehealthspan.com/download/4-Thyroid1.1.doc

It simply says increase until body temp is 98.2, OR until you begin to have symptoms of excess thyroid. If you end up with hyper symptoms and your temp isn't up, then there are probably other underlying issues such as poor adrenal function, low ferritin, low b12, etc...(all of which should be checked before going on such a protocal).

If temp returns and stays normal, cycling isn't required.

[JanSz]

The last page of this document (a link you posted earlier) specifically states the treatment is to ramp up until body temp is too high, then ramp down.

From a health perspective no-one should ramp up their T3 until their body temp is too hot, and then maintain that level of T3 - that's unhealthy. Therefore this is obviously designed to be implemented by ramping up and then immediately ramping down.

http://www.ehealthspan.com/download/4-Thyroid1.1.doc


The Australian pharmacist confirms this point about Wilson's Therapy, in the link I posted earlier, ie:

http://www.custommedicine.com.au/blog/2007/04/17/reverse-t3-dominance/


The 98.2F temperature that is quoted by dr Rothenberg in treatment of Wilson’s syndrome is hardly a high temperature.

There is debate going on on what constitutes normal body temperature.

Depending on geograhic locations and locations on the body, the numbers vary, but are always within range of (36.6C-37.0C)=97.88F-98.6F)

I think dr Rothenberg just picked number that is right in the middle of that range.

With, hopefully, high temperature anxiety behind us, I think it may be important to spend some time at that temperature range (being fed with T3), so the reset mechanism (that we are after) have a time to take place. This is the 2-3 months (quote below).

Ideally that temperature (98.2F or close to it) will continue after T3 is withdrawn. If temperature does not stay at that level, dr Rothenberg advices or another cycle of T3.
.
================================================== =====
37.00 98.60
36.95 98.51
36.90 98.42
36.85 98.33
36.80 98.24
36.75 98.15
36.70 98.06
36.65 97.97
36.60 97.88
===============================
http://www.custommedicine.com.au/blog/2007/04/17/reverse-t3-dominance/
We have found that by using a
consistent low dose of T3 over
two to three months
without the need of cycling the dose, as described by Dr Wilson,
in addition to addressing the causes of improper T4 metabolism,
many patients have responded favorably with improved symptoms and a reduction in reverse T3 levels.
===============================

=================================================
=================
I would feel more comfortable if I could have more indicators than just a temperature.
I have picked top range of FreeT3(230-420)pg/dL, because that is the best that I can come up with.
Not about RT3, but I started with low body temp, ( 35.85C= 96.53F) and low FreeT3.
Went to Armour Thyroid, watched pulse and temperature, ended at 3grains.
3grains Armour--->114mcg(T4), average body production of T4(90-100)
My pulse in 70's bpm and temperature 36.60C=97.88F
but FreeT3 was over the top range

Until I have a better way, when treating RT3 I would add condition
FreeT3<=420 pg/dL

[Drew]

The 98.2F temperature that is quoted by dr Rothenberg in treatment of Wilson’s syndrome is hardly a high temperature.

There is debate going on on what constitutes normal body temperature.

Depending on geograhic locations and locations on the body, the numbers vary, but are always within range of (36.6C-37.0C)=97.88F-98.6F)

I think dr Rothenberg just picked number that is right in the middle of that range.

With, hopefully, high temperature anxiety behind us, I think it may be important to spend some time at that temperature range (being fed with T3), so the reset mechanism (that we are after) have a time to take place. This is the 2-3 months (quote below).

Ideally that temperature (98.2F or close to it) will continue after T3 is withdrawn. If temperature does not stay at that level, dr Rothenberg advices or another cycle of T3.
.
================================================== =====
37.00 98.60
36.95 98.51
36.90 98.42
36.85 98.33
36.80 98.24
36.75 98.15
36.70 98.06
36.65 97.97
36.60 97.88
===============================
http://www.custommedicine.com.au/blog/2007/04/17/reverse-t3-dominance/
We have found that by using a
consistent low dose of T3 over
two to three months
without the need of cycling the dose, as described by Dr Wilson,
in addition to addressing the causes of improper T4 metabolism,
many patients have responded favorably with improved symptoms and a reduction in reverse T3 levels.
===============================

.


Agreed Jan. 98.2 is definitely not a high temp. Although a t3 only protocal is something I currently don't do, I do see merit for some. As far as I'm concerned, I ran a daily temp of 96.0-97.0 for years. I now average about 98.4 daily, on 4 grains of armour.

[JanSz]

]


Agreed Jan. 98.2 is definitely not a high temp. Although a t3 only protocal is something I currently don't do, I do see merit for some. As far as I'm concerned, I ran a daily temp of 96.0-97.0 for years. I now average about 98.4 daily, on 4 grains of armour.

Between what dr John says (max 3grains Armour)
biological data (body produces 90-100mcg T4)(3grainsArmour=114mcg(T4)
and my own experience,
I strongly suggest monitoring
FreeT3
and do not use Armour dose that would make your
FreeT3>420pg/dL
.
By following this I do not expect your body temp to go lower than it currently is
36.90C=98.40F

or, you should be ok if you are less than 98.4F but >=36.6C=97.88F

=============================================
With all above said,
when I was on 3grainsArmour my FreeT3=483pg/dL
and I did not feel any worst or better when I got down to 2.5grains.
So, that final adjustments may be just cosmetical
.
.

[chilln]

[QUOTE=chilln;32025]The last page of this document (a link you posted earlier) specifically states the treatment is to ramp up until body temp is too high, then ramp down.QUOTE]

Just for clarification, it doesn't state to ramp up until body temp is too high. What it states is this:

• Compounded extended release T3 7.5 mcg q12 hours x 2 days
• If oral temp not 98.2 increase to 15 mcg q 12 hours x 2 days
• Increase till 98.2 or symptoms of thyroid excess
• Then taper back at same rate
• Then temp should stay normal or another cycle required

http://www.ehealthspan.com/download/4-Thyroid1.1.doc

It simply says increase until body temp is 98.2, OR until you begin to have symptoms of excess thyroid. If you end up with hyper symptoms and your temp isn't up, then there are probably other underlying issues such as poor adrenal function, low ferritin, low b12, etc...(all of which should be checked before going on such a protocal).

If temp returns and stays normal, cycling isn't required.


Good point. I was focusing on the cyclic part, and I only included one of the two "if...then" conditions (temp / excess thyroid symptoms).

My point about Wilson's Therapy being cyclic still stands.

[chilln]

The 98.2F temperature that is quoted by dr Rothenberg in treatment of Wilson’s syndrome is hardly a high temperature.

OK, 98.2 is not too hot for some. I'm not going to stress over that one.

Dr Wilson's Therapy is cyclic.

A non-cyclic mechanism of increasing T3 for an extended period, to address high reverse T2 , is not Dr Wilson's therapy. It is "someone else's" therapy.

[chilln]

[QUOTE=chilln;32025]If temp returns and stays normal, cycling isn't required.

A ramp up to a situation of "thyroid excess", followed by an immediate ramp down, is in this context, a single cycle of a multi cycle process.

Ie: if it doesn't nail it the first time, then repeat (ie: add an additional cycle) until it does.

From the way these people discuss repeat cycles, they expect repeat cycles.

###

I suspect you believe that most people will only ever need a single cycle. I doubt it, but then none of us have tried it.

I'm still in favor of the Australian pharmacist's method of increasing T3 for a sustained period.

###

I suspect some people who pay serious attention to their symptoms and who are prepared to measure their body temperature in several places to determine a broader view, will do well on a cyclic therapy - even if they only ever have to undergo a single cycle.

But I doubt that most of those people with high reverse T3, would be able to manage this reliably.

We have a hard enough time getting forum members to even chase their medical professional advisers to acquire reverse T3 via labs.

The odds that those who are:
a) lucky enough to have a medical professional adviser who is attentive enough to measure reverse T3,
are also
b) extremely attentive to detail (ie: monitoring temp and symptoms reliably)
is relatively low.

[JanSz]

http://anabolicminds.com/forum/male-anti-aging/66268-jans-bloodtest-april13-5.html#post1703242

Safety Precautions for Thyroid Hormone Therapy
http://www.thyroidscience.com/letters/letters.htm#Safety_Precautions_for_Thyroid_Hormone _Therapy
--------------------------------


http://www.drlowe.com/QandA/askdrlowe/mostrecent.htm#November%
Dr. Lowe
criticises Dr. Dennis Wilson’s theories but admits that using T3 works.

But he does not like sustained-release T3, best use of T3.

.

[Kydd]

I know of people who HAVE done T3 only protocol to clear RT3..... my wife included.

Some gradually go back to Armour after the protocol and do fine. Others stay on T3 only because the issues they suspect caused/contributed to the RT3 in the first place have not been or cant be resolved. In my wifes case Mercury from her Amalgams interferes with T4==>T3. She was too ill until recently to even consider removing them. Now that she is doing better we will look at whether we can do something about them.

My wife was on "T3 only" for 4 months until RT3 suddenly cleared & minor Hyperthyroid symptoms appeared. She was one of those prepared to take temps 4 times a day, and monitor BP & HR, journal symptoms meds doses etc. She got to 150mcg T3 (Tertroxin) stopped for several days when Hyper symptoms appeared & restarted on 80mcg daily (multidosed). Testing of RT3 near the end of that 4 months showed RT3 was now undetectable.

She remains on that 80mcg dose & has been for a couple of months now. She is doing MUCH better since doing this protocol & losing weight as well. She had been on Aussie "Armour" (Thyroid Extract USP) for almost 2 years prior to this. Adrenals, Sex Hormones, Nutrition, Vit & Mineral levels etc had all been optimised prior to T3 protocol with NO resolution of RT3 problem.

There are in fact many doing this protocol & achieving success in the main. They are NOT doing Wilsons meaning they are NOT cycling the T3. Rather they are doing similar to what the Aussie pharmacist suggested. In fact my wife printed that info out & showed her Doc to consider if Armour wasnt successful. They also find SRT3 & even compounded T3 does not work as well as commercial T3 like Tertroxin & Cytomel.

[hardasnails1973]

using normal t3 is just the same as TR t-3. more so people that have absorption issues are more effected with TR formula.

[JanSz]

I know of people who HAVE done T3 only protocol to clear RT3..... my wife included.

Some gradually go back to Armour after the protocol and do fine. Others stay on T3 only because the issues they suspect caused/contributed to the RT3 in the first place have not been or cant be resolved. In my wifes case Mercury from her Amalgams interferes with T4==>T3. She was too ill until recently to even consider removing them. Now that she is doing better we will look at whether we can do something about them.

My wife was on "T3 only" for 4 months until RT3 suddenly cleared & minor Hyperthyroid symptoms appeared. She was one of those prepared to take temps 4 times a day, and monitor BP & HR, journal symptoms meds doses etc. She got to 150mcg T3 (Tertroxin) stopped for several days when Hyper symptoms appeared & restarted on 80mcg daily (multidosed). Testing of RT3 near the end of that 4 months showed RT3 was now undetectable.

She remains on that 80mcg dose & has been for a couple of months now. She is doing MUCH better since doing this protocol & losing weight as well. She had been on Aussie "Armour" (Thyroid Extract USP) for almost 2 years prior to this. Adrenals, Sex Hormones, Nutrition, Vit & Mineral levels etc had all been optimised prior to T3 protocol with NO resolution of RT3 problem.

There are in fact many doing this protocol & achieving success in the main. They are NOT doing Wilsons meaning they are NOT cycling the T3. Rather they are doing similar to what the Aussie pharmacist suggested. In fact my wife printed that info out & showed her Doc to consider if Armour wasnt successful. They also find SRT3 & even compounded T3 does not work as well as commercial T3 like Tertroxin & Cytomel.

Kydd;
I am glad that your wife is getting good help.
IIRC dr Lowe stated that slow release T3 is ng, he also prefers normal T3.
I am assuming that one would have to dose it much more frequently, 4x/day??
Skipping any cycling and staying on T3 only (for much longer time) make also more sense.

You have already provided lots of details, would you mind adding anything else that may be missing?
Something that when presented to our doctors and may look as complete procedure to him.
What kind of blood tests, what goals?

While on Armour Thyroid, I use FreeT3 to establish my dose.
T3,Free(230-420)pg/dL
goal being upper 1/8 of range up to or even slightly over it.
Watching body temperature and heart rate.

I imagine, that while on T3 theraphy, one would monitor at least

T3, Total
T3, Reverse
T3, Free

What are the goals?
I think that limitations about FreeT3 should still apply (yes??).

Describe your wife's history of body temperature.
How it correlates with:
T3 dose size
RT3
anything else

What is her temperature now?
------------------------------------------
.
.

[Kydd]

Hi Janz,

I will have to get the exact protocol from my wife & get back to you.

Just an aside my wifes temps initially were very high. In fact they would have normally indicated a fever. However she did not have a fever , had no illness or infection, was chilled with cold feet & hands and was heat & cold intolerant.

Difficult to get the temperature of a room right for her actually:biggrin:

She eventually tested as low Aldosterone/Sodium. After Florinef, Sea Salt and RX Potassium ther electrolytes were optimised . This fixed the related symptoms she had (BP dropping on standing, frequent peeing, nocturnal peeing, headaches, reduced edema, light sensitivity, tinnitis, noise sensitivity, etc).

What was interesting was it also finally revealed her "true" Hypothyroid LOW temps especially her basal temps!!!

Back later with more "protocol" details.

[JanSz]

Hi Janz,

I will have to get the exact protocol from my wife & get back to you.

Just an aside my wifes temps initially were very high. In fact they would have normally indicated a fever. However she did not have a fever , had no illness or infection, was chilled with cold feet & hands and was heat & cold intolerant.

Difficult to get the temperature of a room right for her actually:biggrin:

She eventually tested as low Aldosterone/Sodium. After Florinef, Sea Salt and RX Potassium ther electrolytes were optimised . This fixed the related symptoms she had (BP dropping on standing, frequent peeing, nocturnal peeing, headaches, reduced edema, light sensitivity, tinnitis, noise sensitivity, etc).

What was interesting was it also finally revealed her "true" Hypothyroid LOW temps especially her basal temps!!!

Back later with more "protocol" details.

Very interesting.
I am glad that you wife was able to find helpful doctor.
Rare breed.
You may want to post his name.

Waiting for details.

.

[thenxtgrt1]

Hi Janz,

I will have to get the exact protocol from my wife & get back to you.

Just an aside my wifes temps initially were very high. In fact they would have normally indicated a fever. However she did not have a fever , had no illness or infection, was chilled with cold feet & hands and was heat & cold intolerant.

Difficult to get the temperature of a room right for her actually:biggrin:

She eventually tested as low Aldosterone/Sodium. After Florinef, Sea Salt and RX Potassium ther electrolytes were optimised . This fixed the related symptoms she had (BP dropping on standing, frequent peeing, nocturnal peeing, headaches, reduced edema, light sensitivity, tinnitis, noise sensitivity, etc).

What was interesting was it also finally revealed her "true" Hypothyroid LOW temps especially her basal temps!!!

Back later with more "protocol" details.

Update?

[JanSz]

http://forum.mesomorphosis.com/mens-health-forum/thyroid-question-dr-m-134269499.html

http://musclechatroom.com/forum/showthread.php?p=35167#post35167

================================================== ========
My summary of dr marianco's post:


Total T4 can be used as a ceiling for how much T4 can be given.
Similarly with T3.
With thyroid, Free T3 is actually a useful tool, ........
When combined with Total T4, Total T3, and Free T4,
and the patient's signs and symptoms,
this is all that is needed.
TSH in this case is not needed.

Cheers.
================================================== ========

An incredible well written post from Dr M. It might deserve a stick

When interpreting thyroid function, it is very important to obtain a Total T4.
T4 is about 98 percent of circulating thyroid hormone.

If one is treated with T3 (Liothyronine, Triiodotyronine), then Total T3 will also be important to determine what is occurring.

Thus a more complete thyroid panel would include:
Free T4, TSH
Free T3
Total T3
Total T4

One reason total values are important is that the free levels are influenced by the availability of the various thyroid binding proteins - such as albumin, thyroid binding globulin, and transthyretin.

These binding proteins are influenced by other factors, such as:
Albumin - hydration, general nutrition
Thyroid binding globulin - estrogen signaling strength
Transthyretin - vitamin A signaling strength (since it not only binds T3 preferentially but also viltamin A)

The binding protein levels are not accounted for by the free levels of T3 or T4. Thus when other factors come into play, they will directly interfere with or complicate interpretation.

Additionally, you have weakly bound versus strongly bound interactions with the binding proteins - just as Albumin vs. SHBG have weak vs. strong binding to testosterone. (This is why total testosterone is the best measure overall of testosterone signaling strength.)

Total T4 can be used as a ceiling for how much T4 can be given. Similarly with T3.

Free T4 is not a sensitive indicator of total thyroid signaling strength.

Free T3 is one indicator of total thyroid signaling strength, but I would also take into account Total T4 since thyroid can also be converted within certain cells to T3 prior to use.

Using Free T3 without a total T4 (and Total T3 if needed) to determine thyroid hormone dosing is like flying blind in fog. There is no indication of the endpoint. It would be like using Free Testosterone to determine how much testosterone to give.

In addition to lab tests, it would be important to also try to establish physical markers as targets when doing thyroid replacement therapy. This would include reduction or correction of signs of thyroid hormone deficiency. When one can establish physical markers/signs to determine thyroid dosing, it can be as sensitive or as good as lab tests. This is how physicians did it prior to the development of lab tests.

Combining both physical exam and lab testing would be ideal though patients may not have the means for frequent lab testing. Thus the choice of labs needs to be tailored to the patient and their circumstances.

Winter is a particularly stressful time. One factor is colder weather which forces an increase in sympathetic nervous system activity. This may lead to a reduction in serotonin signaling. This then may result in a reduction in thyroid hormone production. Additionally, the stress resulting from cold weather may result in adrenal fatigue, which would result in a reduction in T4 to T3 conversion. Lower vitamin D levels - as it is used up from fat stores in darker light - also may result in a reduction in serotonin signaling, resulting in a reduction in thyroid hormone production. Stress may also result in zinc loss, impairing thyroid hormone production. Stress also increase insulin resistance, leading to a renal loss of iodine, possibly impairing thyroid hormone production.
Assuming the nervous system is working well enough (a huge assumption) to:
1. monitor thyroid hormone signaling well
2. produce TSH well
then certain doses of thyroid hormone replacement do not necessarily result in a lower TSH.

There are many factors involved. For example:

1. Does the additional exogenous thyroid hormone lead to suppression of thyroid hormone production such that there is more or equivalent loss of thyroid hormone than addition of thyroid hormone? This lead to TSH remaining the same or going higher.

2. Does the additional thyroid hormone lead to stress on the adrenal glands and adrenal fatigue? Or is there already adrenal fatigue, which can be worsened by the addition of thyroid hormone? If so, then thyroid hormone activation from T4 to T3 is impaired. This would increase TSH or break even and keep TSH the same.

3. Does the additional thyroid hormone trigger metabolic signaling pathways such that thyroid binding hormones are increased? This would lead to the same or lower free thyroid levels. TSH would then either remain the same or increase.

4. etc. etc.

Note that one alternative way to do thyroid hormone replacement is to deal directly with the hormone levels, forgetting about TSH. TSH varies much between people and actual thyroid hormone levels and it makes a huge assumption that the nervous system is functioning well enough to appropriately monitor thyroid levels and appropriately produce TSH (despite aging, for example). Thus TSH in many people (such as those with metabolic illnesses, heart disease, diabetes, mental illness, etc.) is not a good measure of thyroid function. This method is analogous to doing testosterone replacement. Who determines testosterone level based on LH or FSH? Hardly any one. It is easier to dose testosterone based on total level than by monitoring LH and FSH levels. With thyroid, Free T3 is actually a useful tool, unlike Free Testosterone (which reflects SHBG which is determined by a multitude of hormone signals). When combined with Total T4, Total T3, and Free T4, and the patient's signs and symptoms, this is all that is needed. TSH in this case is not needed.

.

[chilln]

My summary of dr marianco's post:



I thought that you were trying to avoid any discussion of generic thyroid stuff, and that you were trying to keep this thread specific to high reverse T3.

I'm worried that if there's a problem addressing reverse T3, then all you're going to do is measure what Dr Marianco's post recommends:
free T3
free T4
total T3
total T4
TSH.
(and no need to measure reverse T3, because Marianco did not include that in his post)

###

You may want to stick to your original plan ?

I know a few people who are dying to discuss all of the thyroid issues which we should all attend to first, but which you didn't want to discuss - sort of like Dr Marianco's info above.

[JanSz]

purpose of this post is to store information

--------------------------------------------------------------------------------
http://musclechatroom.com/forum/showpost.php?p=35413&postcount=2


Better than TSH, T4. Also T4 only preparations not the best, according to this JCEM paper:

http://74.125.47.132/search?q=cache:zm9S202Eb0wJ:www.holtorfmed.com/nss-folder/printable_pdf/thyroid/reverse_r3_%2520thebest.pdf+reverse+t3&cd=2&hl=en&ct=clnk&gl=us&client=firefox-a

This is very nice find, rick055, thank you.
From the link you posted I got to:

http://www.holtorfmed.com/nss-folder/printable_pdf/thyroid/reverse_r3_%20thebest.pdf

They say that their position is based on

The Journal of Clinical Endocrinology & Metabolism 2005; 90(12):6403–6409
here is the link to it:
http://jcem.endojournals.org/cgi/reprint/90/12/6403.pdf
---------------------------------------------------------------------
Holtorf Medical Group, INC
I summarize their position, which is:

higher T4 levels were associated
with decreased peripheral conversion of T4, low T3 levels and high rT3

rT3 inversely correlates with physical performance

T3/rT3 ratio is currently the best indicator of tissue levels of thyroid

-----------------------------------------------------------------------
I underline the T3/rT3 ratio because (I think) I disagree with that position.
My disagrement is on a basis of my reading the original document, that is:
The Journal of Clinical Endocrinology & Metabolism 2005; 90(12):6403–6409

In the Journal they newer made claims about T3/rT3.
But they posted TABLE 2 on a page #3.
Using mean values from that table for T3 and rT3 I calculated T3/rT3 ratio for all cases listed in that table.

T3/rT3 ratio is for:
All subjects---4.3
No diseases---4.5
One disease---4.7
Two diseases---4.3
Three or more diseases---4.1

I note that this ratio is rather flat and inconclusive,
and totally different from a value of 10 that is quoted in many places.
=================================================
///////////////////////////////////////////////////////////////////////////////////////////////
But looking at Fig 1, page #4, the healty people (elderly men) are in upper left quadrant.

T3>1.35 nmol/L=87.7 ng/dL
rT3< 0.32 nmol/L=20.8 ng/dL

also Fig 2
gives desirable FT4 & RT3 ranges

RT3(0.12-0.32)nmol/L=(7.8-20.8)ng/dL

FT4(11-25)pmol/L=(0.85-1.94)ng/dL


/////////////////////////////////////////////////////////////////////////////////////
================================================== ======
http://health.groups.yahoo.com/group/RT3_T3/files/
file name
Examples of How to Calculate FT3/RT3 and TT3/RT3 Ratios

**post 26633, calc by Val**

I have not checked (yet) how this guidelines would correspond to my (JanSz) findings (above in blue) (but they can't be all that bad).

The ratio calculated should be greater than 20 for FT3/RT3 and greater than 10 for T3/RT3.


Also, in a text form, how to calculate those ratios:
http://f1.grp.yahoofs.com/v1/MKIeSyqhzeQecXhHeFAZUQ2qFk-F8UEHzGVjVFU9MGkkCLGrk3J0IgJFnIXQfiUXKVJ7Wv246eWvl 8bDN0R2k0Nw75o/ExamplesofHowtocalculateratio.txt
================================================== ======
convert T3 nmol/L to ng/dL

1.35 nmol/L=1.35/0.0154=87.7 ng/dL
0.32 nmol/L=0.32/0.0154=20.8 ng/dL
================================================== ======
I am always comparing to my own health status to gain perspective.
My known values, are unfortunately not from same blood draw.

rT3=23.1(9.0-35.0)ng/dL (midrange is 22ng/dL)

T3,Total=165(60-181)ng/dL (I was on 3Grains of Armour)
================================================== ======
My bottom line conclussion.

Proper thyroid upkeep must include rT3 check.
rT3 must be at least in lower half of its range.
when supporting thyroid with Armour Thyroid it may be a our good luck that Armour contains relatively more T3 that healthy human produce.
It may be a not bad idea to add little extra T3 while taking Armour.
================================================== ======
To convert Thyroxine, free (T4) readings:-
Divide pmol/L by 12.87 to get ng/dL (nanograms per decilitre)
Multiply ng/dL by 12.87 to get pmol/L (picomoles per litre)

To convert Thyroxine, total (T4) readings:-
Divide nmol/L by 12.87 to get µg/dL
Multiply µg/dL by 12.87 to get nmol/L


To convert Triiodothyronine free (T3) readings:-
Divide pmol/L by 0.0154 to get pg/dL
Multiply pg/dL by 0.0154 to get pmol/L

To convert Triiodothyronine total (T3) readings:-
Divide nmol/L by 0.0154 to get ng/dL
Multiply ng/dL by 0.0154 to get nmol/L

================================================== ======

http://musclechatroom.com/forum/showpost.php?p=49156&postcount=45

---------------www.youtube.com/watch?v=ojY9QE5y_uI&feature=PlayList&p=0CE3727A9805E841&index=4&playnext=2&playnext_from=PL

Changing patterns of hormones with aging - Eugene Shippen

.========================
links:

http://health.groups.yahoo.com/group/RT3_T3/links

attachment #3 have a blue line, it corresponds to requirement that

The ratio should be greater than 10 for T3/RT3

....

[chilln]

http://jcem.endojournals.org/cgi/reprint/90/12/6403.pdf

The Journal of Clinical Endocrinology & Metabolism 2005; 90(12):6403–6409

higher T4 levels were associated
with decreased peripheral conversion of T4, low T3 levels and high rT3



But Dr Marianco didn't say that.

So Dr Marianco's post is general thyroid info which is unrelated to reverse T3.

Therefore general thyroid info is fine to stick in this thread.

[rick055]

"higher T4 levels were associated with decreased peripheral conversion of T4, low T3 levels and high rT3"

This is interesting as it suggests what to me would be counter intuitive: they noticed when there was more raw material (Total T4) there was less active metabolite (T3) and more inactive metabolite (rT3).

To me it seems not just an argument for a T4/T3 med vs straight T4, but also one which supports the 4.22:1 ratio found in Armour.

[JanSz]

888888888888888888888888888



hello jan,

i am from spain, so, in advance, sorry for my poor english.

Since you are my teacher and i have already learned many things from you, i would like to expound you my personal point of view about the following question. You said:

"after we check

iodine
iodide
selenium
copper
zinc

what else can we do to make d1 happy?"
=======================
-----
hgh is the answer. It burns t4 like crazy.

Few weeks ago my free t4 was 0.76 ( 0.60 - 1.60 ) on 2 1/2 grains of thyroid-s and a bit of hgh.

Nevertheless, my average body temperature was 97,8 - 98,0.

I have (like you) midrange rt3. Needed cytomel??

The answer is no. I was on 30-35 mg hc for many months. Don't work for me. Instable temperatures and more. Last week i switched to methylprednisolone + dexamethasone and voila!: My temperatures are now between 98,3 - 98,5.

Hence for me: Hgh to convert t4 to t3 (besides dhea, iodine, etc) and stronger steroid than hc to push t3 into de cells.

Btw i am 51 yo, panhypopituitary.

Thank you so much for your knowledgeable advices on this and other forums.

Mike(edited)

pd.- i can provide you more details if interested.
hi mike/(edited);

you are wery kind.
i am not a medical doctor, just doing my own research, most often i use those results for my own health benefit. So far it works good.

I would like to post your obserwations on my thyroid thred if that is ok with you.
They are interesting and logical.
Others may benefit.
--------------------------------------------------
if you have more thyroid tests it would help.
From the way you have described your thyroid situation i woud say that you were not bad temperature wise to begin with.
97.8f=36.56c
98f=36.67c
then you changed from
hc-hydrocortisone
to
methylprednisolone + dexamethasone
so your temperature raised to
98.3f=36.83c
98.5=36.94c
what makes you think that gh had anything to do with this raise of temperature?
Possibly there was different sequence or more details.
When changing two variables at the same time it is hard to judge which one is dominant.

One warning;
30-35 mg hc for many months
and now even more efficient methylprednisolone + dexamethasone

may cause a bone loss.

Make sure at at some time you check your bones in two ways:
One is dexa scan to check your current balance
the other is;
collagen cross-linked n-telopeptide (ntx), 24-hour urine (36421x)
to check if you loosing any bones now.

--------------------------------------------------

i am 69yo. 5'9" 160#
i have a lipo-sarcoma cancer in my left thigh.
My surgeon in famous cancer institute, sloan kettering cancer institute in manhattan, told me that i should not use growth hormone because sarcoma and gh have affinity.

Hormones are not this surgeon's specialty, so i am looking for a good reason why i should be allowed to use gh.

Suzan sommers have a brest cancer, she uses gh.

If you come accross some information that sounds hopefull (and reliable), please let me know.

Cheers.
Jan
.
.



hello jan,

note that my temps "97.8 - 98" were on 2 1/2 grains of thyroid-s. Not bad, but not optimal.

what makes you think that gh had anything to do with this raise of temperature?

the temperature raise was for the stronger steroid used. The gh works increasing the t4 to t3 conversion rate (i assume it is by increasing the d1 activity).

Some history:

2008-april (no meds)

tsh: 1,69 (0,27 - 4,20)
ft4: 1,31 (0,93 - 1,70) (49%)
ft3: 3,02 (1,80 - 4,20) (50%)
rt3: 0,24 (0,15 - 0,35) (45%)

comments: It sounds to me like hormones floating (pooling) in the blood. Ft4: Low conversion rate; ft3: Insufficient cortisol to push it into the cells. Low temps. Dehydrated. Hypopit.

2008-sept (2 grains thyroid-s; 30 mg hc; no hgh)

tsh: 0.07
ft4: 0,90 (0,70 - 1,48) (25%)

comments: Not ft3 nor rt3. Average temps: 36.4 - 36.6c

2009-feb (2 1/2 grains thyroid-s; 30-35 mg hc; 0.2 mg hgh = 0.6 iu)

ft4: 0,76 (0,60 - 1,60) (16%)

comments: Increased thyroid-s + hgh = lower than ever ft4. Temps didn't change. Maybe t3 pooling around.

2009-mar (only changed steroid: 4 mg mp + 0.1 mg dex)

no labs. Temps raised (daily average) to 36.8 - 36.9 c. Low cortisol symptoms disappeared.

i am using "genotonorm miniquick" pfizer. Prescribing information warnings about the increasing conversion of t4 to t3.

Personal conclusions: It seems like hgh is increasing conversion of t4 to t3 and hc is too weak for me. I need a stronger steroid to cope with cortisol deficit.
================================================== ==========

thank you for your warning about bone loss.

I began hc on 2008-august. I had dexa scan (here "densitometría ósea") one month later, on september.
Result: "osteoporosis".
No way hc being the cause.
I think steroids binds calcium in the digestive tract but i doubt very much that physiological doses can produce or worsen osteoporosis.
My current hc equivalent steroid dose is 23 mg, maybe 24 adding 0.1 mg fludrocortisone. Nevertheless, i am keeping alert.

================================================== =======

sorry for your lipo-sarcoma. Pfizer prescribing information says that treatment of tumoral activity must be finished at the time of beginning gh supplementation. I think your best bet will be to visit a especialist in gh therapy doctor. Sorry, cannot help more.

================================================== =======

i would like to post your obserwations on my thyroid thred if that is ok with you.

it is ok (but, please, do not show my spanish name)

================================================== ===

btw, your eod schedule (t + hcg) works wonder.

kind regards,

mike(edited)

[JanSz]

http://www.vademecum.es/medicamento/clasificacion-terapeutica/D/856/21107/1/1/4/4/advertencias-y-precauciones/genotonorm.html

During treatment with somatotrophin, there has been an increase in the conversion of T4 to T3, which may cause a reduction in serum concentrations of T4 and increased serum T3 concentrations.

In general, the peripheral thyroid hormone levels have been maintained in the reference ranges in healthy subjects.

The effects of somatotrophin on thyroid hormone levels may be relevant in patients with subclinical central hypothyroidism in which theoretically can develop hypothyroidism.

By contrast, in patients receiving thyroxine replacement therapy, mild hyperthyroidism may occur.

It is therefore particularly advisable to check the thyroid function after starting treatment with somatotrophin and after dose adjustments.

In patients with growth hormone deficiency secondary to treatment of malignant diseases is recommended to pay attention to signs of relapse of the tumor.
=================================
=================================

http://www.emea.europa.eu/pdfs/human/referral/genotropin/347703en.pdf

I got this link thanks to Mike, thank you.
Document in above link have a lots of nice information on GH/thyroid/cancer/dosing size/etc
Document is in PDF format and protected.
Only printing is allowed and fst web view.

I want to copy some of the text.
I can save a printer file.
How to get copy of part of the text, not necessarily formated.
I hate to type so much text.

[Mike]

More about HGH increasing conversion of T4 to T3 (AND DECLINE IN RT3 LEVELS):

Effects of growth hormone therapy on thyroid function of growth hormone-deficient adults with and without concomitant thyroxine-substituted central hypothyroidism.

http://www.ncbi.nlm.nih.gov/pubmed/2685007


Thyroid function during growth hormone therapy

http://tinyurl.com/d7ftec



"Finally, five studies in hypopituitary patients have revealed a decline in T4 concomitant with an increase in T3 during GH therapy for between 2 weeks to 18 months (...). Rezvani et al. (1981) also reported a decline in RT3 levels, which put together suggested a GH-induced enhancement of extra thyroidal T4 to T3 conversion."

Growth Hormone in Adults: Physiological and Clinical Aspects
Anders Juul and Jens O.L. Jorgensen
Cambridge University Press, 2000
Page 335

http://tinyurl.com/dgta6g



Interesting read:

"If you’ve been using GH without T4, you’ve been wasting half your money – and if you’ve been using it with T3, you’ve been wasting your time. Start using T4 with your GH, and you’ll finally be getting the full results from your investment."

http://www.anthonyrobertsonline.com/articles/thyroid_hormone.html
.
.
.

[hardasnails1973]

There has been an ongoing to debate for years about this.
One guy says t-3 only, another on saids tricana (t-4) only, another one says take both. SO true fact is that gh increases d1 which converts t4 to t3 so in retrospect from this information then t4 would be the proper therapy PROVIDED THE ADRENALS ARE FUNCTIONING OPTIMALLY NOT CONVERTING TO RT3

[JanSz]

There has been an ongoing to debate for years about this.
One guy says t-3 only, another on saids tricana (t-4) only, another one says take both. SO true fact is that gh increases d1 which converts t4 to t3 so in retrospect from this information then t4 would be the proper therapy PROVIDED THE ADRENALS ARE FUNCTIONING OPTIMALLY NOT CONVERTING TO RT3


Test and verify, double or tripple important when using GH.
GH definitely alters thyroid panel (per manufacturers research).
But more Total-T3 and FreeT3 is beneficial (to a point).
I can think of three primary goals when looking at thyroid panel.

rT3< 0.32 nmol/L=20.8 ng/dL (from research on old men, needs to be refined, (number lowered?))
FreeT3~400pg/dL
Total-T3 in mid range or up to a top range

Since GH increases conversion T4-->T3
I assume that some people (on GH) may see high Total-T3
If the Total-T3 gets close to the top range, I suggest at some point withdrawing Armour(T+T3) (or Synthroid-T4) and transition to Cytomel-T3
People who do not need any thyroid supplementation (plenty of own T4) prior to GH use, may find themself with excessive RT3, T3, FreeT3.
So, I see thyroid readings as one of the reasons to limit upper GH dose.
------------------------------------------------------------------------------
I assume that prolonged time when
T4~zero
RT3~zero
is not harmfull

Is that true?
================================================== ====
rT3< 0.32 nmol/L=20.8 ng/dL
derived in post #47
.
.

[JanSz]

http://forum.mesomorphosis.com/mens-health-forum/thyroid-question-dr-m-134269499-2.html#post622102
=======================================
http://forum.mesomorphosis.com/621918-post18.html

One simple way to target thyroid replacement is as follows:
Assuming there are no significant major health problems and nutrition is optimized,
use T4 or Armour Thyroid, and/or T3 to gradually achieve the following:

First: Total T4 between 8-12. Generally midway is better to avoid over-conversion to T3 when the adrenals are working well.

Second: Free T3 between 3.4 to 4.2. Generally midway is better to avoid adrenal fatigue from high free T3). Avoid high Free T3 - backing off the T4 target if T4 to T3 conversion is too strong.

Once this is achieved, then any remaining problems associated with thyroid are due to conversion problems from T4 to T3, e.g. such as due to adrenal fatigue, excessive stress, end-organ thyroid resistance, the other signaling systems, etc.. In this case, address adrenals, address nutrition, address stress, improve sleep, psychological problems, see specialist, etc.

Nutrition absolutely has to be optimized to avoid serious health problems with thyroid.
Of course, consult with your physician before undergoing any thyroid treatment.

Levothyroxine has an advantage here since it can increase Total T4 to its target most easily, without overly stressing the adrenal glands.

This is analogous to Total Testosterone as a target for testosterone replacement - as I have posted before.

ADRENAL FATIGUE:
The adrenal glands give out not only
cortisol, but also
pregnenolone,
DHEA,
progesterone,
testosterone,
aldosterone,
estrogen, etc.

As the adrenal glands fatigue, they will try to keep cortisol production up while progressively sacrificing production of the other signals. Thus, cortisol alone is NOT a good measure. The other signals also have to be monitored to determine what state of fatigue one has.
Cortisol can be "normal" yet the adrenal glands can be fatigued as shown by deficiencies in the other signals. This is why in some, Cortisol is still necessary for supportive treatment.

This is why I don't advocate monitoring Cortisol alone. The spectrum of signals needs to be measured to determine its status.

This is analogous to using only fasting blood sugar or hemoglobin A1c alone as a monitor for insulin resistance or diabetes. This doesn't tell much unless it is seriously off. One has to monitor fasting insulin, cortisol, lipids, thyroid, etc. etc. to get a better picture of what is happening. For example, one can have a "normal" blood sugar but have an insulin level of 200. This indicates severe insulin resistance and a pancreas that is working very hard to control blood sugar. When the pancreas fails to do this, then glucose goes out of control and diabetes may occur. This would not be shown by only testing hemoglobin A1c or fasting glucose.

Cheers.
Dr. M
================================================== ==========

http://forum.mesomorphosis.com/622102-post21.html

I believe "Adrenal Fatigue" exists. It is one of the contributing factors to many illnesses.

Regarding Wilson's Syndrome, I keep an open mind. However, there isn't much evidence for it, as far as I know.

Interestingly, one intervention used historically in psychiatry is to give a person with treatment resistant depression a short course of T3 (25 to 50 mcg). This, in some, kick starts their antidepressant treatment. And some patients improve. This is all done without lab measurements.

One problem I see with Wilson's Syndrome is that thyroid hormone levels decline with age. Thus at some point, if patients want to optimize their treatment and health, chronic thyroid treatment will still have to be used if a patient has physical and/or lab signs for hypothyroidism. Physiologic levels can be relatively low by the time one is in one's 30's. These can be seen in the difference in physical signs and performance when comparing one's self between the 20s and 30s.

Higher Reverse T3 levels primarily indicate that the person has other health problems, not just thyroid problems. These other health problems - inadequate nutrition, disease, excessive stress (including adrenal fatigue and mental illness), excessive immune system activity - will have to be addressed to optimize health.

If one is focusing solely on thyroid hormone replacement or optimization, then Reverse T3 is not a central issue. This is analogous to testosterone replacement, where libido is actually not a focus. Testosterone is only one factor in improving libido. Libido is determined by numerous factors which also have to be addressed, not only testosterone. Few patients who see me, for example, for problems with libido, have low testosterone. In testosterone replacement, the primary goal is achieving a target total testosterone (such as 650 ng/dl). Once done, any remaining problems are not due to testosterone. The other causes have to be found and addressed.

Reverse T3 is primarily produced from T4 by deiodinase D3. T3 is primarily produced from T4 by deiodinase D2. Thus if one is worried about Reverse T3, then one has to worry more about the deiodinase enzymes and what factors will inhibit D2 and promote D3 production. Further, one will have to worry about what will inhibit D2 versus promite D3 activity. And so on. It becomes a huge hornet's nest or gordian knot with few known entry points to make adjustments.

If anything, these adjustments are not often with thyroid replacement. For example, inflammatory cytokines or excessive oxidative stress can promote D3 and inhibit D2. This means one should reduce one's stress, treat any infections, address adrenal fatigue, improve one's nutrition to improve antiinflammatory signaling and reduce oxidative stress, etc. Note again that these interventions aren't thyroid hormone.

In some select patients, T3 treatment is useful - particularly if there is some thyroid hormone resistance or problems in converting T4 to T3. I don't like using it alone if the doses are high, however, since T3 is cleared so quickly compared to T4. Further, T3 used alone can suppress T4 production down to zero. What if the patient loses their bottle of T3 on a trip? I prefer pairing it with Armour or Levothyroxine to maintain a reserve of T4 to stabilize overall thyroid signaling as T3 goes up and down through the day.
Cheers. Dr. M

[JanSz]

Thyroid hormones transport and metabolism

Endocrine toxicology - Google Book Search (http://books.google.com/books?id=URc5JMoNirgC&pg=PA51&lpg=PA51&dq=albumin+thyroid&source=bl&ots=g9k2uzFdag&sig=SvIjQqr4mCkzQzF9y-92HV20vEI&hl=en&ei=4mjFSbbZMInDtwexuMzJCg&sa=X&oi=book_result&resnum=3&ct=result#PPA52,M1)

But I think the problem (if any) may be in your 40% rolercoaster rather than the level itself.

The BAt that you posted looks real good to me, but it probably fluctuates the same as your TT.
.
================================================== =====

http://books.google.com/books?id=AV_7ltX0WEAC&pg=PA201&lpg=PA201&dq=replace+50+micrograms+of+T4+with+12.5+microgram s+of+T3&source=bl&ots=vRhaB5phv7&sig=JUhauz9SndxyDH7tjJqFKiyUjaM&hl=en&ei=d33JSbjGPNjHtgftvbCjAw&sa=X&oi=book_result&resnum=10&ct=result#PPA112,M1

Living well with hypothyroidism By Mary J. Shomon

It is searchable.
================================================== ======
Basic & clinical endocrinology By Francis S. Greenspan, David G. Gardner

http://books.google.com/books?id=DH99-QrGAPEC&pg=PA59&lpg=PA59&dq=SHBG+tbg+regulation&source=bl&ots=DdzkCTGveG&sig=_A11h4i75_-gJhQBVi7fJM_mw8E&hl=en&ei=IYjJSbSVIaGstgevhZ2VAw&sa=X&oi=book_result&resnum=1&ct=result

It is searchable.
================================================== ========

[chilln]

All that Marianco is saying is that don't single out high reverse T3 as the first problem which needs addressing.

Ie: address other issues first, including general thyroid hormone imbalance, and after any quick wins to those areas have been realized, and if high reverse T3 is still an issue, then address high reverse T3 by supplementing with a combination of T4 and T3 which is tailored for the individual (not necessarily the exact ratio as in Armour).

I believe we already follow this practice, (I follow this practice) but if any of us are still not following this practice, then we should re-assess our strategy.

[Dr. John Crisler]

Please do not take this thread off track.
This thread is about high RT3.
When RT3 is sufficiently high, others call it
Wilson’s reverse T3 dominance syndrome.

I have open #2 thread because the first one was side-tracked.

Please open new thread and we will discuss other aspects of thyroid treatments, worthy topic.

When discussing (on this thread) please assume that the (good) points raised by HAN are already accounted for by treating provider and RT3 is still very high.
.
.That IS the answer, friend, not "off track". HAN pushing the nutritional approach is dead on.

[Dr. John Crisler]

This is a second thread about RT3.
We already have been thru the "usual"
selenium, zinc, Vit B6, B12 and E, iron and iodine supplements.
So lets assume that we have done due diligence in that area.
-------------------
Reason why T3 is supplemented:
existing T3 will reduce TSH, TSH-->0
when TSH~0 then T4 is not produced
after certain time (2-3 months?) T4 is depleted, T4~0


After the theraphy ends new T4 arrives.
Supposedly, when starting a new the enzymes D1 & D3 work at proper (or better) proportions.

It is explained better here:

http://www.wilsonssyndrome.com/WhyIsIt.htm
http://www.wilsonssyndrome.com/Medical.htm
http://www.wilsonssyndrome.com/SiteMap.htm

WTS appears to be due to a bogging down of the thyroid system due to impaired T4 to T3 conversion. This bogging down of the thyroid system appears to be perpetuated by RT3 in the tissues, as well as perhaps other factors. Once the system is bogged down, it appears that backlogged raw thyroid hormone (T4) can also adversely compete with the active thyroid hormone (T3). Even though T4 is the source of T3, if it's not being converted well it can actually be a significant hindrance!
Wilson's T3 protocol is aimed at depleting RT3 levels in the tissues of the body, for a time. This is accomplished by reducing T4, its only source. T4 is reduced by reducing TSH (Thyroid Stimulating Hormone). TSH is reduced by giving patients pure T3 directly.

When patients are given pure T3 directly, their bodies sense that they are getting enough thyroid stimulation so they reduce their own production of thyroid hormones.

The purpose of the treatment is not so much to give patients' thyroid glands a rest (although that does happen), as it is to clear RT3 (by clearing T4) out of the tissues so that their thyroid systems can get de-bogged, cleaned out, and reset. This appears to be what enables the patients' thyroid systems to function well on their own again. Wilson's T3 therapy does not need to be taken for life, rather usually only a few weeks or months.
================================================== ========
=======================
http://www.wilsonssyndrome.com/WhyUndiagnosableWithThyroid.htm

wilsonssyndrome.com/WhyUndiagnosableWithThyroid

Hearing about the importance of T4 to T3 conversion and RT3, some physicians and labs have started looking at Total T3, Free T3, Total T4, Free T4, Total RT3, and T3/RT3 ratios. But none of these tests demonstrate T4 to T3 conversion in the tissues and cells of the body. They only show what's floating around in the blood stream just like any other blood test. Some doctors and labs are starting to tell people that there are new tests unlike the normal thyroid tests that can confirm or deny WTS. But that's not true. Some doctors and labs are saying, in effect, "OK conversion, let's measure T3 and RT3 in the blood." However, presenting and relying on a new line of inconclusive thyroid blood tests that replaces the first would just be putting us right back where we started. This explains why many patients still respond extremely well to the treatment regardless of what any of these tests say. Not only do some of the patients with "normal" tests still respond well, but so do some that are shown as being "abnormal" in a way that's supposedly exactly opposite to WTS. For example, some of the patients with "low" RT3 levels and/or "high" Free T3 levels and/or high T3/RT3 ratios can still respond beautifully well to the WT3 protocol.I'd like an explanation--including facts--for this statement.

[JanSz]

----------------------------------------------------------------------
http://forum.mesomorphosis.com/newreply.php?do=newreply&p=623216


TSH generally can have a wide variation in range. Using it as a measure also assumes a lack of serious comorbid illness and an intact and fully functioning nervous system. This may often NOT be the case. And thus TSH becomes a poor measure of thyroid function. In the original studies on TSH, the range of actual values was so wide when one looks at the raw data, it is a wonder it was chosen as a measure of thyroid activity. Hardly anyone uses LH or FSH to determine total testosterone, why should the same be true of TSH? Both come from the pituitary.

Low T4, Low T3, high Free T3, High Free T4 may mean low thyroid binding proteins are low.

One of the functions of binding proteins (such as SHBG and Thyroxine Binding Globulin) is to prolong the half-life of the substance bound. For example, testosterone has a half life as little as 10 minutes. If so and if there was no SHBG, then nearly all of one's testosterone would be destroyed in about 50 minutes!

For example, when high insulin levels (such as in diabetes type 2) lower SHBG, testosterone's half-life is reduced, and testosterone concentration goes down. This is a vicious circle since lowering testosterone also reduces insulin sensitivity, which leads to higher insulin production from the pancreas to compensate. There may be normal or high Free Testosterone under this circumstance. But Free Testosterone does not represent total testosterone signaling well. Loosely bound and strongly bound testosterone also have signaling activity or function (as in the SHBG-testosterone combination binding to SHBG receptors).

Likewise, lower thyroid binding proteins (Thyroxine Binding Globulin, Transthyretin, Albumin) reduce the half-life of thyroid hormone resulting in lower total thyroid hormone levels. Lower thyroid binding proteins also results in a higher proportion of the free hormone.

The converse example also works. For example, estradiol stimulates the production of Thyroxine Binding Globulin. This causes total thyroid hormone levels to increase - at times past the usual reference range. However, there is less Free T4, possibly less Free T3 (which is also bound by Transthyretin and thus may be less effected). This causes a relative hypothyroidism in the person, and a higher TSH. This is why estrogen-containing birth control pills can contribute to weight gain or mood instability should the woman be sensitive to higher estrogen levels.

In regard to sub-physiologic cortisol treatment, Cortisol is subject to negative feedback inhibition. Total cortisol is determined usually by the brain's needs for cortisol production, generally determined by sympathetic nervous system activity. When one administers a subphysiologic dose of cortisol, total cortisol is expected to generally remain the same since the addition of exogenous cortisol would lower the adrenal production of cortisol, thus creating a balance. If cortisol is absorbed very quickly, creating a peak that is supraphysiologic, then total cortisol, for a moment may be higher.

Generally, adding cortisol alone may cause problems because it lowers the production of all of the adrenal cortex products. Thus, there may be a deficit of DHEA, progesterone, testosterone, estradiol, etc. In sum, these may promote thyroid signaling. Thus TSH may go up. Additionally, should stress increase as a result of this deficit, insulin resistance may go up, possibly resulting in an eventual loss of thyroid production. Cortisol, itself, can cause a transient drop in diodinase 2 activity, reducing T4 to T3 conversion. However this may not last more than a day.

The story gets more complicated as one delves more deeply. When you can see most of the web of signals and how they interact, your head can spin.

In regard to Arimidex, it is an option in controlling estradiol. The long half-life makes it important to have patience since a single change can take 4-6 weeks to stabilize. It is, however, a very expensive an option.

Addressing adrenal function may not address insulin resistance fully since it has multiple other causes.

Cheers.
------------------------------------------------------------------------

7 keto dhea
http://forum.mesomorphosis.com/623203-post3.html


DHEA is the most common hormone the body makes, by amount. However, its conversion to testosterone and estradiol can be a significant problem for some patients (though not all).

Women, for example, very often can't use high DHEA doses even if needed to obtain decent DHEA concentrations (e.g. past 12.5 mg a day of a good, active DHEA tablet). They may get acne and hair loss as side effects of the androgenic signaling of DHEA. Thus, I would use 7-KETO DHEA plus or minus a small amount of DHEA. Some men too readily convert testosterone to estradiol and thus may get excessive estradiol from DHEA.
7-KETO DHEA is a metabolite of DHEA which doesn't further metabolize to testosterone and estradiol. But it has many of the non-reproductive hormone benefits of DHEA. It appears to improve cellular immune system activity, reduce diastolic blood pressure, reduce triglycerides, improve thyroid hormone signaling (such as by improve T3 levels), reduce insulin resistance, improve metabolic rate, reduction in sympathetic nervous system activity (i.e. reduction in stress), improvement in mood, potentially improvement in memory, etc.

Potential downsides include increasing IL-2 an inflammatory signal and immune system activity - but this I suppose is offset by decreases in inflammatory signaling by its other actions - otherwise excessive inflammatory processes would be a concern (e.g. exacerbation of arthritis, asthma, allergies, etc.). If anything, patients with inflammatory illnesses have already excessive immune system activity. If it isn't compensated, a person's inflammatory status needs to be monitored and compensated via other signaling systems or nutrition. Insomnia may occur if dosed at night - depending on the person. Increasing thyroid signaling excessively is also a problem if already on thyroid replacement. This can lead to palpitations, heart problems, and adrenal fatigue. Nutrition has to be optimized to help offset adverse effects.

Usually the best time for it is in the morning. Dosing is usually between 5-200 mg a day. The lower doses may be effective depending on the person. 7-KETO has a half-life of 2.2 hours. Thus in some people, twice a day dosing may be more beneficial.

7-KETO DHEA is a good alternative to DHEA particularly those sensitive to reproductive hormone conversions from DHEA. The dose has to be individualized by clinical effect since targetting by blood levels is not generally done. It can be combined with DHEA.

Cost and availability was a significant concern in the past. But more companies now produce it and the cost has become more reasonable.

Cheers.

[chilln]

JanSz - this also applies to you, it's not just a response to Dr Crisler.




I'd like an explanation--including facts--for this statement.


This has become JanSz's "filtered RSS feed" (ie: one-way traffic) for Marianco's comments which are completely without their original context - and therefore in this forum Marianco's statements appear only as generalizations.

I suspect that Marianco's original statements, when read in their original context, are likely to be addressing a specific individual's circumstances, and therefore persons reading Marianco's statements in their original context are better able to derive the exceptional circumstances when they apply.

But if Marianco's statements are indeed generalizations, then I can guarantee that they don't apply to all people at all times - not even the vast majority.

And since most of us have at least one unusual response to a supplement, which is a function of our individual genetics, therefore I don't agree with dumping these generalizations here, on the assumption that "they apply to most of us and that we should believe them without question."

By allowing these generalizations to be placed here, out of their original context, and without entering into any sensible discussion re their applicability, we are allowing "lecturing".

A forum can technically be anything at all, but in this context I'm suggesting that we do not allow this thread to continue to be a "filtered RSS feed" for Marianco's statements, while discussion re those comments is shunned or avoided by JanSz.

####

People can setup a login to Mesomorphosis, and any other forum where Marianco participates interactively, and they can read Marianco's statements in their correct context, and they can quiz Marianco re those comments, and Marianco will no doubt then tailor a response to the individual.

####

JanSz, I believe you would not necessarily be able to back up some of Marianco's more complex statements on your own, and you are not even responding to Dr Crisler himself.

If you want to setup a site where a filtered subset of Marianco's comments can be stored for posterity, then I recommend you negotiate with a Web Hosting provider, and setup your own domain and your own site.

I also suspect that Marianco himself would have his own terms and conditions, so would best consult with Marianco too.

So what's your angle ?

And please notice how my post (this post) is part of a discussion, not a "filtered feed" from Mesomorphosis.

[JanSz]

http://www.armourthyroid.com/con_faqs.aspx#q4

The basic "rule of thumb" in converting thyroid doses is that
100 mcg of T4 is roughly equal to 25 mcg of T3, or 1 grain (60 mg) of Armour Thyroid.



Drug | Thyroid Tablets, USP (Armour® Thyroid) | Liotrix Tablets, USP (Thyrolar®a) | Liothronine Tablets, USP (Cytomel®b) | Levothyroxine Tablets, USP(Unithroid®c, Levoxyl®d, Levothroid®e, Synthroid®f) |
Approx. Dose Equivalent | 1/4 grain (15 mg) | 1/4 | | 25 mcg (.025 mg) |
Approx. Dose Equivalent | 1/2 grain (30 mg) | 1/2 | 12.5 mcg | 50 mcg (.05 mg) |
Approx. Dose Equivalent | 1 grain (60 mg) | 1 | 25 mcg | 100 mcg (0.1 mg) |
Approx. Dose Equivalent | 1 1/2 grains (90 mg) | 1 1/2 | 37.5 mcg | 150 mcg (0.15 mg) |
Approx. Dose Equivalent | 2 grains (120 mg) | 2 | 50 mcg | 200 mcg (0.2 mg) |
Approx. Dose Equivalent | 3 grains (180 mg) | 3 | 75 mcg | 300 mcg (0.3 mg) |


Endocrinology Articles
http://emedicine.medscape.com/endocrinology

[JanSz]

http://books.google.com/books?id=mRG2g91DbxUC&pg=PA295&lpg=PA295&dq=t3+t4+hal+flife&source=bl&ots=I-TkB1oVwv&sig=RiIpk7L6v-ag_vJJpsiZmBY1FFU&hl=en&ei=e8DwSdL2JNbgtgex3626Dw&sa=X&oi=book_result&ct=result&resnum=10#PPA295,M1

Thyroid Basics

Thyroid releases thyroid hormone 80% in form of T4 and 20% in form of T3

T3 is the primary active hormone

T4 is metabolized to T3 at the tissue level by tissue deiodinases, including type 1 deiodinase

Type 2 deiodinase is found primarily in brain/pituary,
metabolizes T4--->T3

Type 3 deiodinase metabolises
T4--->reverseT3(rT3)
which is hormonally inactive

................................................

lets fish out Type 3 deiodinase

http://www.google.com/search?q=type+3+deiodinase&rls=com.microsoft:en-us:IE-SearchBox&ie=UTF-8&oe=UTF-8&sourceid=ie7&rlz=1I7GGLL_en
.................................................. ..



http://www.newmanveterinary.com/ThyroidBasics.html

[rick055]

Type 3 deiodinase metabolises
T4--->reverseT3(rT3)
which is hormonally inactive



Which means it doesn't oppose the action of T3??

[JanSz]

Which means it doesn't oppose the action of T3??

That, I think is old news and probably true only in very limited way.
---------------------------------------------------------------------
I am still searching, but it looks like:

High RT3 is due to high (level or activity) of Type 3 deiodinase

High Type 3 deiodinase is a sign of cancer (except in fetal tissue and placenta).


the last piece is even more bad news than the first.
--------------------------------------------------------

It looks like most of articles that I can google are very recent and accessable by ($$$$) subscription only.

lets google on:

Type 3 deiodinase

.
.

[JanSz]

http://anabolicminds.com/forum/male-anti-aging/66268-jans-bloodtest-april13-5.html#post1982080
post #136

http://forum.mesomorphosis.com/mens-health-forum/low-ferritin-low-thyroid-134273298.html
================================================== =======
ferritin
hemochromatosis
marianco


Without iron, the metabolic actions triggered by thyroid hormone grind to a halt. No ATP, not cellular metabolism.

Thyroid hormone replacement does not work well without adequate iron levels - best measured by serum Ferritin levels.
=============================
For people with confirmed hemochromatosis
Iron Overload Diseases Association, INC.
confirmed by all three tests as shown here:
http://www.ironoverload.org/diagnosis.html

Ferritin: 5 to probably 50.
http://www.ironoverload.org/anemia.htm
--------------------------
For people with out hemochromatosis
desired ferritin boundary (75-150)ng/dL
with preference toward higher end.
================================================== ====
.

I am sorry that it took me 7 years to nail it down.
For you guys who have attention of high class doctors
all above is an old news (yeah right).
I was starring with blind eyes at my ferritin=28
.

[rick055]

Have you started supplementing? Anything to report?

[JanSz]

Have you started supplementing? Anything to report?

Week ago I had drawn blood for my long list, expect results by end of next week, will go from there.

I already have little history about my ferritin.

With out any supplementation my ferritin as posted, ferritin=28

I was using 4 pills/day of iron pills from LEF, blood test, ferritin=54

at that time I stopped using iron pills because I read the recomendations from
Iron Overload Diseases Association, INC. (ferritin(5-50))

But now I understand those recomendations better, thanks to dr Marianco.

I newer tested for hemachromatosis, but now I did.
I have a good chance of not having it.
I will be eating iron pills by handfulls.
Over the years I had 7 surgeries with anastesia, that probably contributed to my low iron.

Must admit that while raising ferritin 28-->54
I did not feel any difference.

I am constantly looking for more energy.
Not that I am letargic, but always would like to push for more.
I am sure my 69th birthday few days ago have nothing to do with it (fingers crossed).
==========================================

Note:
I will have to investigate the issue further.
Phlebotomist hinted that for such a large amount of vials of blood I could/should get prepared as for blood donation, get the blood out and distribute to vials.

Did not had opportunity to ask for more details.
>
>

[rick055]

I am constantly looking for more energy.
>
>

I can sympathize.

Have you checked adrenals?

[JanSz]

I can sympathize.

Have you checked adrenals?

I have this on my list:

35 --------- DHEA Sulfate 402X
36 --------- Aldosterone
37 --------- ACTH, Plasma
38 --------- Cortisol Binding Globulin (Transcortin) (37371X)
39 --------- Cortisol AM/PM

/

[chilln]

Without iron, the metabolic actions triggered by thyroid hormone grind to a halt.

When you combine all these rules together you soon realize that hormone management therapy really is as complex as rocket science.

No wonder so many medical professional advisers find it so difficult.

[JanSz]

When you combine all these rules together you soon realize that hormone management therapy really is as complex as rocket science.

No wonder so many medical professional advisers find it so difficult.

At this moment I am looking at iron as my way of increasing my energy level.
Yet I worry, because it took lots of iron pills (4/day over many months) to get minimal raise 28-->54
yet I did not felt any difference in energy level or otherwise.
Constipation for first 2-3 week, nothing else.
Unless my comming blood test report will tell me otherwise, I am planning to go for 6 pills/day.

I have LEF's
Iron Protein Plus 300 mg, 100 capsules Item Catalog Number: 563

Any suggestions???

.

[chilln]

At this moment I am looking at iron as my way of increasing my energy level.
Yet I worry, because it took lots of iron pills (4/day over many months) to get minimal raise 28-->54
yet I did not felt any difference in energy level or otherwise.
Constipation for first 2-3 week, nothing else.
Unless my comming blood test report will tell me otherwise, I am planning to go for 6 pills/day.

I have LEF's
Iron Protein Plus 300 mg, 100 capsules Item Catalog Number: 563

Any suggestions???

.


This is obviously a genetic weakness. 4 caps of LEF's Iron Protein plus is a huge amount of highly absorbable iron (absorbable in everyone else except you).

Your body is not making an enzyme necessary to absorb the iron in LEF's formulation.

I know you take digestive enzymes, but perhaps you take the iron without your digestive enzymes, and perhaps you need some protease along with the "iron protein" to release the protein bound to the iron ?

[JanSz]

This is obviously a genetic weakness. 4 caps of LEF's Iron Protein plus is a huge amount of highly absorbable iron (absorbable in everyone else except you).

Your body is not making an enzyme necessary to absorb the iron in LEF's formulation.

I know you take digestive enzymes, but perhaps you take the iron without your digestive enzymes, and perhaps you need some protease along with the "iron protein" to release the protein bound to the iron ?

I should have mentioned that without taking iron my stool is light in color.
With iron it is dark brown, apparently I am not absorbing iron.

Thank you for suggestion---protease

Do you happen to have a link to your favorite protease, please.

But in the mean time with my
Iron Protein Plus 300 mg, 100 capsules Item Catalog Number: 563
http://www.lef.org/Vitamins-Supplements/Item00563/Iron-Protein-Plus.html

I will be taking

Enhanced Super Digestive Enzymes with Probiotics
100 vegetarian capsules
Item Catalog Number: 01273
http://www.lef.org/Vitamins-Supplements/Item01273/Enhanced-Super-Digestive-Enzymes-with-Probiotics.html

containing:
Protease II (from papain) (43,333 USP/mg or 7,800 PU) 18 mg
Protease III (60,000 FCC/gm or 1,300 HUT) 22 mg



.
.

[chilln]

I should have mentioned that without taking iron my stool is light in color.
With iron it is dark brown, apparently I am not absorbing iron.

Thank you for suggestion---protease

Do you happen to have a link to your favorite protease, please.

But in the mean time with my
Iron Protein Plus 300 mg, 100 capsules Item Catalog Number: 563
http://www.lef.org/Vitamins-Supplements/Item00563/Iron-Protein-Plus.html

I will be taking

Enhanced Super Digestive Enzymes with Probiotics
100 vegetarian capsules
Item Catalog Number: 01273
http://www.lef.org/Vitamins-Supplements/Item01273/Enhanced-Super-Digestive-Enzymes-with-Probiotics.html

containing:
Protease II (from papain) (43,333 USP/mg or 7,800 PU) 18 mg
Protease III (60,000 FCC/gm or 1,300 HUT) 22 mg



.
.

I've PM'd you re my protease source

[spiderRico]

Is this Wilson's protocol only good if your temp is low? What if you have normal temps, but high rt3? Is it still effective in cleaning up the rt3?

[JanSz]

Is this Wilson's protocol only good if your temp is low? What if you have normal temps, but high rt3? Is it still effective in cleaning up the rt3?

I would say yes.

I do not know, and do not want to know, what you call Wilson's protocol.
People get hung up on names.
What I did is continous, steady, daily doses.

I just got my blood test results and am sitting on them studying.

Previously,
2.75Grains of Armour Thyroid

RT3=23.1(9-35)ng/dL---(middle of range=22)
T3,Total=165(60-181)ng/dL
T4,Total=10.2(4.5-12.0)ug/dL

------------------------------------
I switched to
25mcgCytomel(T3) + 20mcgCytomel(T3) + 1.5GrainArmour

RT3=12(11-32)
T3,Total=205(97-219)ng/dL
T4,Total=4.1(4.5-12.0)ug/dL

================================================== ======

[spiderRico]

I would say yes.

I do not know, and do not want to know, what you call Wilson's protocol.
People get hung up on names.
What I did is continous, steady, daily doses.

I just got my blood test results and am sitting on them studying.

Previously,
2.75Grains of Armour Thyroid

RT3=23.1(9-35)ng/dL---(middle of range=22)
T3,Total=165(60-181)ng/dL
T4,Total=10.2(4.5-12.0)ug/dL
------------------------------------
I switched to
25mcgCytomel(T3) + 20mcgCytomel(T3) + 1.5GrainArmour

RT3=12(11-32)
T3,Total=205(97-219)ng/dL
T4,Total=4.1(4.5-12.0)ug/dL

================================================== ======
Thanks Jan,
I'm just going from the link you gave in the original post. They called it WT3, Wilsons t3 protocol.

[JanSz]

Thanks Jan,
I'm just going from the link you gave in the original post. They called it WT3, Wilsons t3 protocol.

There was nothing personal in my response.
I apologise if you took it that way.

I am learnig along the way.
If I would call what I did WT3 protocol, there would be six guys telling me that what I did was something else.
But in the mean time I had little high RT3 and want to figure out how to get it down.
I do not want to get bug dow in semantics, I am not a scientist, I just want to have my RT3 in good place.

Since you also have high RT3, my experience may give you some idea.

Unfortunately I am missing quite few thyroid related items that I have requested.
The report is still hot from the press.
I will study it and ask doc for those missing items.

.
.

[spiderRico]

There was nothing personal in my response.
I apologise if you took it that way.

I am learnig along the way.
If I would call what I did WT3 protocol, there would be six guys telling me that what I did was something else.
But in the mean time I had little high RT3 and want to figure out how to get it down.
I do not want to get bug dow in semantics, I am not a scientist, I just want to have my RT3 in good place.

Since you also have high RT3, my experience may give you some idea.

Unfortunately I am missing quite few thyroid related items that I have requested.
The report is still hot from the press.
I will study it and ask doc for those missing items.

.
.

Didn't take it in the wrong way at all. Was really just thanking you for your response. Just was explaining why I called it that.

[JanSz]

Posted for reference;

Note the basic supplements that needs to be checked for good thyroid support.

http://www.futureformulations.com/store/thyro-balance-tm-p20.html


Ingredients - Thyro-Balance™ contains a special liquid blend of:
calcium,
chromium,
iodine,
magnesium,
manganese,
selenium,
zinc,
vitamin A,
beta-carotene,
vitamin B 1,
vitamin B 2,
vitamin B 3,
vitamin B 5,
vitamin B 6,
vitamin B 12,
folic acid,
biotin,
vitamin C,
bioflavonoids,
vitamin D,
vitamin E complex,
boron &
choline, in a base of L-tyrosine, & liquefied seaweed with citrus seed extract.

================================================== ===========
http://www.stopthethyroidmadness.com/aldosterone/

Florinef dosing/related, posts

http://musclechatroom.com/forum/showthread.php?t=3637&page=5

#42, #45, #50

suppress TSH when hashi antibodies

.

.........

[pmgamer18]

Here is what happens to me on TRT with HCG takeing Cortef and Armour my RT3 goes up with my Estradiol levels to up my last test my E2 was 38 my shbg is 20 I try to keep my e2 at 15. When ever my E2 goes up this high my RT3 goes up it was 43 ng/dL range 11 to 32 just getting my E2 down in the past brings my RT2 down near the bottom of the range. High E2 mess's with your Thyroid this is a fact.

[JanSz]

Here is what happens to me on TRT with HCG takeing Cortef and Armour my RT3 goes up with my Estradiol levels to up my last test my E2 was 38 my shbg is 20 I try to keep my e2 at 15. When ever my E2 goes up this high my RT3 goes up it was 43 ng/dL range 11 to 32 just getting my E2 down in the past brings my RT2 down near the bottom of the range. High E2 mess's with your Thyroid this is a fact.

E2 levels are hard to control, they go of for no apparent reason.

Thyroid levels will be much more steady/predictable on steady schedule of thyroid hormones.

Post all your thyroid analytes.

You may want to replace some Armour with Cytomel(T3).
You can replace most of Armour with Cytomel(T3) as long as your
TotalT4>bottom of range
You can even go below bottom range on TotalT4, but you would have to
have with you 2-3 months supply of Cytome(T3) and Armour, so you know you would not run out of them,
also short phone line to your doc may help (just in case).

Aiming:

RT3 in lower half of range, TotalT3 in upper 1/3 range
FreeT3~400pg/dL or higher if TotalT3 goal not reached
TotalT4>bottom of range
.

[JanSz]

THIS STUFF IS EXPENSIVE

Polish kishka and beef liver w/onions taste better

But in case someone is desperate......
================================================== =====


Proferrin® $26.08 (every 3 days --- gross)

Proferrin®, 30 11mg tablets / bottle

Proferrin® is Heme iron supplement made from red blood cells. You need much less heme iron to get the same or better absorption than when using 70-125mg of non-heme iron salt supplements.

http://medfutures.com/store/product_info.php?cPath=21&products_id=31&osCsid=3ffc9720cfb65743dcee490b4e91f5f6
========================================

http://www.proferrin.ca/compare.html

Answers to Frequently Asked Questions


What is Proferrin® and what is it used for?
Proferrin® is an oral iron supplement made from heme iron polypeptide. It is naturally sourced from iron derived from bovine hemoglobin and is highly available for absorption. Heme iron is readily absorbed throughout the small intestine and is absorbed better than any other form of iron. Proferrin® is used to treat or prevent iron deficiency anemia.


top

What is iron deficiency anemia?
Iron deficiency anemia is the most common type of anemia and is also known as sideropenic anemia. Iron deficiency anemia occurs when the dietary intake or absorption of iron is insufficient and hemoglobin, which contains iron, cannot be formed. Iron deficiency anemia is the final stage of iron deficiency.


top

Proferrin® is a heme iron but what is the difference between heme and non-heme iron?
The advantages of heme versus non-heme iron can be summarized as follows:

Heme iron is more easily absorbed by the human body.
The absorption of heme iron is not affected by food thus making it more convenient.
It is found in meat, fish and poultry
It has fewer to no side effects
top

How do I take it and what is the recommended dose?
This product should be taken by mouth with a full glass of water with or without food unless otherwise directed by a physician. Dosage is based on you medical condition and response to therapy. Use this product regularly to get the most benefit from it. Recommended dose is 1-3 tablets daily.


top

Are there any interactions with other drugs?
Before using heme iron polypeptide, individuals should tell their pharmacist or doctor if using methydopa or other iron-containing products. Iron supplements can decrease the absorption of drugs such as tetracycline antibiotics, penicillamine, cefdinir, chloramphenicol, levothyroxine, and quinolone antibiotics. Therefore, doses of these medications should be spaced as far as possible. This product may interfere with certain laboratory tests (including test for blood in stool) causing false test results. Make sure laboratory personnel and all doctors know a patient is using this drug.


top

What are the adverse effects associated with Proferrin®?
Constipation, diarrhea, nausea, upset stomach, and stomach/abdominal cramping may occur. The incidence of these adverse effects is less than that of ionic iron. Iron may cause your stool to turn black, an effect that is not harmful. A very serious allergic reaction to this product is rare. Do not use if you have an allergy to cow products.


top

What should I if I missed a dose?
If a dose is missed, take it as soon as noticed. If it is near the time of the next dose, skip the missed dose and resume you usual dosing schedule. Do not double the dose to catch up.


top

What should I do in the case of an overdose?
Accidental overdose of iron-containing products is a leading cause of fatal poisoning in children younger than 6 years. Keep this product out of reach of children. If overdose is suspected, contact local poison control centre or emergency room immediately. Canadian residents can call their provincial poison control centre.


top

Does Proferrin® contain lactose or gluten?
Proferrin® does not contain lactose or gluten.


top

Can I take proferrin® if I'm pregnant or nursing?
As with all oral iron supplements, consult your physician before taking Proferrin during pregnancy or nursing.

top

What size is a Proferrin® tablet?
The tablet is long and narrow with a smooth coating (designed to be easy to swallow) and can be broken or crushed. The tablets are smaller than most multivitamins of a similar shape.


top

What are the storage conditions for Proferrin®?
Store at room temperature between 15-30 degrees Celsius (59-68 degrees Fahrenheit) and away from light and moisture. Do not store in the bathroom.


top

I am a pharmacist. How can I get more information about Proferrin®?
Health professionals may download the following Scientific Info file for further details.


top

Where can I buy Proferrin®?
Proferrin® is available through your pharmacy without prescription or online through our website or by calling Medical Futures Inc directly at 1 866 789 2090.


top

[JanSz]

http://www.thyroidmanager.org/
http://www.thyroidmanager.org/Chapter16/16d-frame.htm

----------------------------------

http://endotext.com/
Endotext.org is the web-based source of information on endocrine disease directed to physicians around the world caring for patients with these problems. It is comprehensive, authoritative, constantly up-dated, un-biased, and available without cost to physicians and trainees. All material may be freely downloaded for personal use.

------------------------------------------


*SECTIONS*** (CLICK* TO* OPEN) | **SECTION EDITORS
**Pituitary Disease and Neuroendocrinology | * Ashley Grossman*
**Diabetes Mellitus and Carbohydrate Metabolism | **Ira Goldfine and Robert J Rushakoff**
**Endocrinology of Male Reproductive | **Robert McLachlan
**Endocrinology of Female Reproductive | **Robert Rebar
**Thyroid Disease- www.thyroidmanager.org | **Leslie J De Groot
**Adrenal Disease and Function | **George Chrousos
**Diseases of Bone and Mineral Metabolism | **Frederick Singer
**Diffuse Hormonal Systems and Endocrine Tumor** Syndromes** | **Aaron Vinik
**Pediatric Endocrinology | **Maria New
**Obesity | **Matthias Tschoep
**Endocrine Disease and Pregnancy | **Bruce R Carr
**Endocrine Testing Protocols | * Hossein Gharib
**Endocrinology of Aging | **Jerome M Hershman
**Continuing Medical Education Programs | **Dace Trence, MD




http://health.groups.yahoo.com/group/RT3_T3/



...........

[JanSz]

While reviewing research on my post #47
http://musclechatroom.com/forum/showpost.php?p=35410&postcount=47

one who likes to have better surviwability chance may want to observe

RT3(0.12-0.32)nmol/L=(7.8-20.8)ng/dL

People who have high RT3 have to use T3 to accomplish this goal.
So far this is a good news.
There is a problem and there is a way to solve it.

There are numerous reasons why one may end up with high RT3.

There are three types- of iodothyronine deiodinase that catalyze the initiation (D1, D2) or termination (D3) of thyroid hormone effects.

News may not be a good news for people using GH.

It looks like the process of converting T4--(D1, D2)-->T3
is need by body.

This article explains it in more detail.
http://mesomorphosis.com/articles/anthony-roberts/thyroid-and-growth-hormone.htm

Bottom line from that article:

Quote:
"If you’ve been using GH without T4, you’ve been wasting half your money – and if you’ve been using it with T3, you’ve been wasting your time. Start using T4 with your GH, and you’ll finally be getting the full results from your investment.
===========================================

Good information for a healthy people, specially those who can make good use of T4 and have no problem making T4---->T3 conversion.

Buy that article does not address people who have high RT3 and must use T3 to control it.
.
.
Actually, this reference:
http://www.thyroidmanager.org/Chapter5/chapter5a.pdf

lists numerous reasons why RT3 may be higher.

-----------

I am not sure yet, but it looks that even if one does not supplement with GH but uses T3,
he may be exchanging

High RT3 problem
for
Low GH problem

.
.

[pmgamer18]

The following is the same thing my Heart Dr. told me about my high RT3 levels a cut and paste from your link.
=====================================
rT3 concentrations are elevated in the postoperative
period.

While reviewing research on my post #47
http://musclechatroom.com/forum/showpost.php?p=35410&postcount=47

one who likes to have better surviwability chance may want to observe

RT3(0.12-0.32)nmol/L=(7.8-20.8)ng/dL

People who have high RT3 have to use T3 to accomplish this goal.
So far this is a good news.
There is a problem and there is a way to solve it.

There are numerous reasons why one may end up with high RT3.

There are three types- of iodothyronine deiodinase that catalyze the initiation (D1, D2) or termination (D3) of thyroid hormone effects.

News may not be a good news for people using GH.

It looks like the process of converting T4--(D1, D2)-->T3
is need by body.

This article explains it in more detail.
http://mesomorphosis.com/articles/anthony-roberts/thyroid-and-growth-hormone.htm

Bottom line from that article:

Quote:
"If you’ve been using GH without T4, you’ve been wasting half your money – and if you’ve been using it with T3, you’ve been wasting your time. Start using T4 with your GH, and you’ll finally be getting the full results from your investment.
===========================================

Good information for a healthy people, specially those who can make good use of T4 and have no problem making T4---->T3 conversion.

Buy that article does not address people who have high RT3 and must use T3 to control it.
.
.
Actually, this reference:
http://www.thyroidmanager.org/Chapter5/chapter5a.pdf

lists numerous reasons why RT3 may be higher.

-----------

I am not sure yet, but it looks that even if one does not supplement with GH but uses T3,
he may be exchanging

High RT3 problem
for
Low GH problem

.
.

[JanSz]

The following is the same thing my Heart Dr. told me about my high RT3 levels a cut and paste from your link.
=====================================
rT3 concentrations are elevated in the postoperative
period.

I am a single person (not a doctor) trying to find what is healthy for me, if that helps anybody else that is gravy.
I am not biased toward anything.
I post good or bad.
I am not paid (or terrorized directly or indirectly) by T4 manufactures (like most doctors).

Everybody knows that surgery increases RT3,
there are many other reasons why RT3 increases.

The other study shows that people with high RT3 are dying
People with low RT3 are living longer.

To me it is exact parallel to testosterone study.
High BAT, live longer
Low BAT, life sucks and then you die

Most doctors look at low testosterone and tell you that you are fine
others tell you that you are crazy trying to supplemant with T.

So far we have not had real discussion on RT3.

I think preventing high RT3 is waiting its turn.
It will be next testosterone or TRT.

---------------

I just found yahoo RT3 group, have you looked there?

http://us.rd.yahoo.com/evt=42879/*http://groups.yahoo.com/group/RT3_T3

http://groups.yahoo.com/group/RT3_T3

I signed up to that group but have a big problem staying there.
anytime someone makes new post there I am getting new e-mail
My e-mail box is getting overwhelmed.
Is there any remedy for that?
I had to drop from other yahoo groups for that reason.
I am not planning to read all those posts,
is there any shortcut or summaries there as it is in STTM?

.

[chilln]

I am a single person (not a doctor) trying to find what is healthy for me, if that helps anybody else that is gravy.
I am not biased toward anything.
I post good or bad.
I am not paid (or terrorized directly or indirectly) by T4 manufactures (like most doctors).

Everybody knows that surgery increases RT3,
there are many other reasons why RT3 increases.

The other study shows that people with high RT3 are dying
People with low RT3 are living longer.

To me it is exact parallel to testosterone study.
High BAT, live longer
Low BAT, life sucks and then you die

Most doctors look at low testosterone and tell you that you are fine
others tell you that you are crazy trying to supplemant with T.

So far we have not had real discussion on RT3.

I think preventing high RT3 is waiting its turn.
It will be next testosterone or TRT.

---------------

I just found yahoo RT3 group, have you looked there?

http://us.rd.yahoo.com/evt=42879/*http://groups.yahoo.com/group/RT3_T3

http://groups.yahoo.com/group/RT3_T3

I signed up to that group but have a big problem staying there.
anytime someone makes new post there I am getting new e-mail
My e-mail box is getting overwhelmed.
Is there any remedy for that?
I had to drop from other yahoo groups for that reason.
I am not planning to read all those posts,
is there any shortcut or summaries there as it is in STTM?

.


Analysis of RT3 is occasionally necessary just like analysis of progesterone is occasionally necessary.

You don't directly try to modulate RT3, just like you don't directly try to modulate progesterone.

You directly modulate the easiest-to-modulate hormones: T, cortisol, E2, insulin (via carb intake, not direct injection), DHEA, GH, T4 and T3, pregnenolone, such that optimum RT3 and progesterone results from the modulation of those primary hormones.

If you aren't prepared to modulate several of the easiest-to-modulate hormones, then you can try to mess around with only T4 and T3 to achieve a satisfactory RT3, but I doubt that will ever be sufficient, because the feedback between the easiest-to-modulate hormones and the thyroid hormones is significant.

RT3 will always remain as significant as (say) progesterone, when dealing with male hormone modulation therapy.

[JanSz]

Analysis of RT3 is occasionally necessary just like analysis of progesterone is occasionally necessary.

You don't directly try to modulate RT3, just like you don't directly try to modulate progesterone.

You directly modulate the easiest-to-modulate hormones: T, cortisol, E2, insulin (via carb intake, not direct injection), DHEA, GH, T4 and T3, pregnenolone, such that optimum RT3 and progesterone results from the modulation of those primary hormones.

If you aren't prepared to modulate several of the easiest-to-modulate hormones, then you can try to mess around with only T4 and T3 to achieve a satisfactory RT3, but I doubt that will ever be sufficient, because the feedback between the easiest-to-modulate hormones and the thyroid hormones is significant.

RT3 will always remain as significant as (say) progesterone, when dealing with male hormone modulation therapy.

RT3 is not talk much about because because the head is still in the sand.

Progesterone, not long ago it was forbidden word allowed to use only when saying how bad it is.

We have to turn over each stone.

Testosterone is easy to modulate, question is how to do it the right way.

RT3 is easy to modulate and large number of people on yahoo group do it successfully.
http://groups.yahoo.com/group/RT3_T3

What I am thinking is;
drawbacks, negatives,

what is better, suffer from high RT3
or
pop few Cytomel pills
do some blood tests
get the numbers in line.

And I am thinking of lining up a whole slew of numbers
not just
singling out one number (RT3) and leave everything else unchecked.

.

[chilln]

RT3 is not talk much about because because the head is still in the sand.


I think you're focusing too much attention on RT3. We only focus on RT3 when we've done a first order balancing of T4 and T3.

Addressing RT3 as a second order hormone issue is not putting our heads in the sand.




Progesterone, not long ago it was forbidden word allowed to use only when saying how bad it is.


I don't look back as see how bad the past was. I'm over the past. It's gone. Siyonara.




We have to turn over each stone.

Testosterone is easy to modulate, question is how to do it the right way.


You've left off cortisol, T4, T3, cortisol, pregnenolone, DHEA and E2 from that statement.




RT3 is easy to modulate and large number of people on yahoo group do it successfully.
http://groups.yahoo.com/group/RT3_T3


Everyone on this forum, who modulates their T, cortisol, T4, T3, DHEA, pregnenolone and E2 also modulates their RT3.

And that's a guaranteed fact, even though they didn't get the labs to prove it.

Just because some chaps on another forum choose to get labs to see how their RT3 changes doesn't make them any more intelligent or less intelligent that the chaps here.




What I am thinking is;
drawbacks, negatives,

what is better, suffer from high RT3
or
pop few Cytomel pills
do some blood tests
get the numbers in line.

And I am thinking of lining up a whole slew of numbers
not just
singling out one number (RT3) and leave everything else unchecked.

.

And what I'm thinking is that we should modulate our hormones only when necessary, and then we should modulate them to a first order using a few supplements, and if that's not sufficient improvement, then we have to go to the second order and monitor additional hormones such as progesterone and RT3 to help us see the more complex picture.

No stress.

This is what we are already doing.

I see no need to change our approach.

[JanSz]

Posted for reference.

http://musclechatroom.com/forum/showthread.php?t=4022&page=2
http://musclechatroom.com/forum/showpost.php?p=49916&postcount=13


The future of cortisol supplementation is not Medrol, it's sustained release cortisol.

http://www.phoqus.com/RNS08030301.aspx

http://jcem.endojournals.org/cgi/content/abstract/94/5/1548


Based on the fact these guys are at state 2 clinical trials, I suspect that if your medical professional adviser considers you may need Medrol for now, then you may not have to remain on it for long.

I feel significant positive difference after switching to Medrol.

Will have no problem switching to Chronocort when it will becomes available.


http://www.phoqus.com/introducing%20chronocort.aspx

Chronocort® – aiming for the right drug, at the right dose, in the right way, at the right time

Chronocort® is a novel oral cortisol replacement therapy under development for the treatment of patients with deficiency of the hormone cortisol. The lead indication for Chronocort® will be congenital adrenal hyperplasia (CAH), which is a serious genetic disorder caused by a deficiency in the enzyme responsible for cortisol production. Subsequent indications will include acquired causes of cortisol deficiency (Addison’s disease and hypopituitarism).

Current standard therapy for patients with cortisol deficiency fails to replicate the natural rhythm of a single rise and gradual fall in cortisol levels over a 24-hour period. The failure to match the body’s natural physiological cortisol requirements results in chronic fatigue, lack of energy, depression, anxiety and impaired libido. Many patients are unable to work. Difficulty controlling patients’ symptoms leads to doctors prescribing stronger and longer-acting steroid drugs, and as a result, patients are often on a knife-edge between under- and over-treatment. Over-treatment brings with it the serious consequences of steroid excess (Cushing's) including weight gain, hypertension, diabetes and osteoporosis. Patients with congenital adrenal hyperplasia suffer from additional hormonal abnormalities due to the loss of the natural cortisol rhythm, leading to virilisation and other symptoms.

Chronocort® comprises a tablet containing hydrocortisone (the synthetic analogue of the natural physiological cortisol hormone) with a unique coating and formulation designed to allow delayed and then sustained release of the hormone, such that it mimics the natural 24-hour production of cortisol in the healthy body. Chronocort® utilises QtrolTM, Phoqus Pharmaceuticals’ proprietary drug delivery technology.



Chronocort® development status
Chronocort® is scheduled for launch in 2009/10, subject to the successful completion of the clinical trials and regulatory approval, and is currently undergoing clinical testing in patients with cortisol deficiency. It already has Orphan Drug Designation for both congenital adrenal hyperplasia and acquired adrenal insufficiency (Addison’s disease, hypopituitarism) in Europe. The company is applying for the same in the US. Orphan Drug Status, if granted upon approval, will provide the company with 10 and 7 years of market exclusivity in the EU and US respectively.

[hardasnails1973]

For love of God Valerie is taking phone calls..bless her soul, but damned are the ones that call LOL.

Elevated Reverse t3 is
1) physical trama inside or outside the body, disturbed mental well being of the person, hidden inflammation.
Depressed people have higher rt3
2) Malfunctoin in the conversion of t4 to t3 due to genetic, nutrient deficiency or imblanace in D2 (please correct me if I am wrong)
3) high cortisol levels for short time or longer term low cortisol levels. Giving cortisol or balancing adrenals the rt3 will deactivate and go back to normal.
4) Other hormonal imbalnaces that may effect the D2 enyzme - estrodial, gh, testosterone,

Lets see how long till I get kicked off this forum LOL

[EIC]

For love of God Valerie is taking phone calls..bless her soul, but damned are the ones that call LOL.

Elevated Reverse t3 is
1) physical trama inside or outside the body, disturbed mental well being of the person, hidden inflammation.
Depressed people have higher rt3
2) Malfunctoin in the conversion of t4 to t3 due to genetic, nutrient deficiency or imblanace in D2 (please correct me if I am wrong)
3) high cortisol levels for short time or longer term low cortisol levels. Giving cortisol or balancing adrenals the rt3 will deactivate and go back to normal.
4) Other hormonal imbalnaces that may effect the D2 enyzme - estrodial, gh, testosterone,

Lets see how long till I get kicked off this forum LOL

This makes a lot of sense. Take care of the things that cause excessive conversion to rT3 and then you avoid the problem in the first place. I note that taking low doses of HC will resolve two of the four avenues you discussed (specifically, hidden inflammation and long-term low cortisol).

What sort of nutrient deficiencies cause an imbalance in D2? Is there a thread on this topic?

Regarding #4, what imbalances do you mean? I know high E2 can down regulate thyroid function. Is that what you mean?

[JanSz]

This makes a lot of sense. Take care of the things that cause excessive conversion to rT3 and then you avoid the problem in the first place. I note that taking low doses of HC will resolve two of the four avenues you discussed (specifically, hidden inflammation and long-term low cortisol).

What sort of nutrient deficiencies cause an imbalance in D2? Is there a thread on this topic?

Regarding #4, what imbalances do you mean? I know high E2 can down regulate thyroid function. Is that what you mean?

Surgery and bad recovery causes elevated RT3.

So what is the solution?
Do not go for surgery,
or is there another suggestion?

Avoid long post surgery recovery difficulties, another good suggestion, right?

Wait as long as you can, until in ICU they will put T3 in your IV, hoping to keep you alive, another good suggestion.

----------------------------------------------------------------------------
It is good policy to try all the basics to keep thyroid in balance,
but what to do when they do not work and RT3 stays high.

Is it better to stand still and hope that some day it will go down
or
take action, (little extra T3 rather than T4)
.

[pmgamer18]

Dam Jan when you say things like this "So what is the solution?
Do not go for surgery,"
If this were true I would not be here today sure to keep your RT3 levels down don't go for surgery just die then you don't have to worry about it.


Surgery and bad recovery causes elevated RT3.

So what is the solution?
Do not go for surgery,
or is there another suggestion?

Avoid long post surgery recovery difficulties, another good suggestion, right?

Wait as long as you can, until in ICU they will put T3 in your IV, hoping to keep you alive, another good suggestion.

----------------------------------------------------------------------------
It is good policy to try all the basics to keep thyroid in balance,
but what to do when they do not work and RT3 stays high.

Is it better to stand still and hope that some day it will go down
or
take action, (little extra T3 rather than T4)
.

[hardasnails1973]

melatonin plays a huge factor into this as well. Currently people that are testing low in zinc I am going to suggest to run melatonin salvia test to see if there melatonin is low. Melatonin is needed to help the conversion of t4 to active t3 hormone.

[JanSz]

Dam Jan when you say things like this "So what is the solution?
Do not go for surgery,"
If this were true I would not be here today sure to keep your RT3 levels down don't go for surgery just die then you don't have to worry about it.

Nothing personal,
just checking options.

Ok, so going fo surgery was no-brainer.

God bless they did not succeeded in killing you after good surgery.
But they did their best trying.

Now,
everybody who have surgery get increased RT3.
That is given.
Those who had heavy duty surgery, get more RT3 then those with lighter surgery.

So what you do now?

Wait and hope that it will go away?

You already did more than most of population in trying to adjust it away with dozens of supplements and medicines.

I listed research made on few hundreds of old men.
Those who had RT3 high----> dies sooner.
Those who had RT3 lower----> are still kicking.

.

[Kydd]

Hi JanSz


just found yahoo RT3 group, have you looked there?

http://us.rd.yahoo.com/evt=42879/*ht...m/group/RT3_T3

http://groups.yahoo.com/group/RT3_T3

I signed up to that group but have a big problem staying there.
anytime someone makes new post there I am getting new e-mail
My e-mail box is getting overwhelmed.
Is there any remedy for that?
I had to drop from other yahoo groups for that reason.
I am not planning to read all those posts,
is there any shortcut or summaries there as it is in STTM?

Simple to fix. For any Yahoo Group first go to Group page. Near top of page almost in middle will see "edit membership". Click on that . On step 2 mark "web only" option. You can then read & post from Group page & will receive no more emails. You also have option to have "daily digest" if you prefer. These are the same options available for ALL Yahoo Groups.

[JanSz]

Hi JanSz



Simple to fix. For any Yahoo Group first go to Group page. Near top of page almost in middle will see "edit membership". Click on that . On step 2 mark "web only" option. You can then read & post from Group page & will receive no more emails. You also have option to have "daily digest" if you prefer. These are the same options available for ALL Yahoo Groups.

Thank you Kydd.

How is your wife doing?

.

[Kydd]

melatonin plays a huge factor into this as well. Currently people that are testing low in zinc I am going to suggest to run melatonin salvia test to see if there melatonin is low. Melatonin is needed to help the conversion of t4 to active t3 hormone.

My wifes Melatonin was low but if she took even 1 mg she felt absolutely terrible & it didnt help her sleep issues at all. She didnt have low Zinc though. What about the fact that Melatonin supposedly lowers Cortisol? Great of you have high Cortisol but pretty terrible if it is low?

I think that was my Wifes problem. She was dxed sometime after this & is now on Prednisolone & HC.

How exactly does Melatonin help with Thyroid conversion HAN? Never heard that before.

By the way my Wife did correct all the issues that we were aware of that can cause RT3 but it still didnt help the RT3 just got worse. She had to go to T3 only & the RT3 Group was helpful in how to do that. Her Doc agreed it was worth doing & she is now much better & remains on T3. She noticed a positive difference even on day one of stopping NTH. Took 4 months though to see major improvements.

Her Doc thinks her Mercury Amalgams interfere with Thyroid conversion. She had to get Thyroid & Adrenal support in place before she would be well enough to even contemplate the stress of dental revision & detox. She will likely be starting that before the end of the year (but doing it slowly not all at once).

[JanSz]

My wifes Melatonin was low but if she took even 1 mg she felt absolutely terrible & it didnt help her sleep issues at all. She didnt have low Zinc though. What about the fact that Melatonin supposedly lowers Cortisol? Great of you have high Cortisol but pretty terrible if it is low?

I think that was my Wifes problem. She was dxed sometime after this & is now on Prednisolone & HC.

How exactly does Melatonin help with Thyroid conversion HAN? Never heard that before.

By the way my Wife did correct all the issues that we were aware of that can cause RT3 but it still didnt help the RT3 just got worse. She had to go to T3 only & the RT3 Group was helpful in how to do that. Her Doc agreed it was worth doing & she is now much better & remains on T3. She noticed a positive difference even on day one of stopping NTH. Took 4 months though to see major improvements.

Her Doc thinks her Mercury Amalgams interfere with Thyroid conversion. She had to get Thyroid & Adrenal support in place before she would be well enough to even contemplate the stress of dental revision & detox. She will likely be starting that before the end of the year (but doing it slowly not all at once).

Supposedly prednisolone is hard
people feel better on

methylprednisolone
Medrol

I have recently switched from
30mg-HC
to
6mg-Medrol

previously I knew when previous dose would wear out,
now smooth sailing
================================================== ===

Equivalent maximum doses (do not take pregnenolone
or any other adrenal supplement that breaks down
into cortisol with these)

cortisone acetate 37 1/2 (weak, not recommended)
hydrocortisone 30 mg
cortef 30 mg
prednisone 7 1/2 mg
prednisolone 7 1/2 mg
triamcinolone 6 mg
methylprednisolone 6 mg
**dexamethasone 1 mg
betamethasone 0.8 mg

[Kydd]

Supposedly prednisolone is hard
people feel better on

methylprednisolone
Medrol

I have recently switched from
30mg-HC
to
6mg-Medrol

previously I knew when previous dose would wear out,
now smooth sailing
================================================== ===

Equivalent maximum doses (do not take pregnenolone
or any other adrenal supplement that breaks down
into cortisol with these)

cortisone acetate 37 1/2 (weak, not recommended)
hydrocortisone 30 mg
cortef 30 mg
prednisone 7 1/2 mg
prednisolone 7 1/2 mg
triamcinolone 6 mg
methylprednisolone 6 mg
**dexamethasone 1 mg
betamethasone 0.8 mg

Yep aware of all that. Medrol (Methylprednisolone) is not available in Australia. Even if it was I would still use Prednisolone as it is MUCH cheaper than Medrol. Prednisolone is NOT harsh on Liver Prednisone on the other hand IS. My Wife needed the Prednisolone badly. Would have had to dose HC every 2-3 hours around the clock she metabolised it that quick. Even with Pred she needed 3 times daily dosing. As you said MUCH smoother & she is doing very well on that. She had used Pred in previous years too but at much higher doses for Fibro flares. Fibro is gone by the way a fantastic thing she was in so much pain before Adrenal meds. So she was familiar with Pred & knew she reacted well to it. Of course she is only taking physiological doses now.

As far as the new med Slow Release Cortisol goes I wouldnt touch that with a barge pole either. No way to tell how an individual will respond to a "slow release" formulation. From what I read very few do well on slow release compounded HC and/or Thyroid meds. So why try an expensive "unproven" new med? Rather stick with what I know works & works well for far less money?

[JanSz]

Yep aware of all that. Medrol (Methylprednisolone) is not available in Australia. Even if it was I would still use Prednisolone as it is MUCH cheaper than Medrol. Prednisolone is NOT harsh on Liver Prednisone on the other hand IS. My Wife needed the Prednisolone badly. Would have had to dose HC every 2-3 hours around the clock she metabolised it that quick. Even with Pred she needed 3 times daily dosing. As you said MUCH smoother & she is doing very well on that. She had used Pred in previous years too but at much higher doses for Fibro flares. Fibro is gone by the way a fantastic thing she was in so much pain before Adrenal meds. So she was familiar with Pred & knew she reacted well to it. Of course she is only taking physiological doses now.

As far as the new med Slow Release Cortisol goes I wouldnt touch that with a barge pole either. No way to tell how an individual will respond to a "slow release" formulation. From what I read very few do well on slow release compounded HC and/or Thyroid meds. So why try an expensive "unproven" new med? Rather stick with what I know works & works well for far less money?

1.5$/day
or
1.3$/day if you can split or crush 16mg pills
thefirstdrugstore.com/item.php?id=3544&said=fmeds

.

[Kydd]

1.5$/day
or
1.3$/day if you can split or crush 16mg pills
thefirstdrugstore.com/item.php?id=3544&said=fmeds

.

Perhaps you did not see when I mentioned Medrol is NOT available in Australia? Prednisolone costs AU$18.95 for 60 x 5mg tabs.Its also avilable in 1 mg tabs which is great for weaning or titrating dose.To try Medrol would have to illegally import from a source & pay in US $. First dont want to do that & second would be VERY expensive & third would risk confiscation & prosecution.

Just for fun I looked up price from a source. Cost was 30 x 16mg for AU$186.81 plus delivery!!!

[JanSz]

Perhaps you did not see when I mentioned Medrol is NOT available in Australia? Prednisolone costs AU$18.95 for 60 x 5mg tabs.Its also avilable in 1 mg tabs which is great for weaning or titrating dose.To try Medrol would have to illegally import from a source & pay in US $. First dont want to do that & second would be VERY expensive & third would risk confiscation & prosecution.

Just for fun I looked up price from a source. Cost was 30 x 16mg for AU$186.81 plus delivery!!!

As long as we live
we have to make choices.

.

[EIC]

melatonin plays a huge factor into this as well. Currently people that are testing low in zinc I am going to suggest to run melatonin salvia test to see if there melatonin is low. Melatonin is needed to help the conversion of t4 to active t3 hormone.

Does that mean that having insufficient melatonin leads to excessive rT3, or that it will just leave a lot more T4 unconverted?

How reliable is the melatonin saliva test?

[chilln]

Yep aware of all that. Medrol (Methylprednisolone) is not available in Australia. Even if it was I would still use Prednisolone as it is MUCH cheaper than Medrol. Prednisolone is NOT harsh on Liver Prednisone on the other hand IS. My Wife needed the Prednisolone badly. Would have had to dose HC every 2-3 hours around the clock she metabolised it that quick. Even with Pred she needed 3 times daily dosing. As you said MUCH smoother & she is doing very well on that. She had used Pred in previous years too but at much higher doses for Fibro flares. Fibro is gone by the way a fantastic thing she was in so much pain before Adrenal meds. So she was familiar with Pred & knew she reacted well to it. Of course she is only taking physiological doses now.

As far as the new med Slow Release Cortisol goes I wouldnt touch that with a barge pole either. No way to tell how an individual will respond to a "slow release" formulation. From what I read very few do well on slow release compounded HC and/or Thyroid meds. So why try an expensive "unproven" new med? Rather stick with what I know works & works well for far less money?


Prednisone and medrol are NOT bioidentical to cortisol. They are man made molecules which are similar to cortisol, but not close enough. This is why they are not metabolized as quickly as cortisol.

Normally, when we want to dose a hormone modulating drug or supplement, we use both symptoms and labs, not just one or the other.

But neither prednisone nor medrol can be measured by a cortisol lab test. And there are no commercial prednisone or medrol lab tests available in any case.

If it were possible (which it is not) we would dose prednisone or medrol reliably by purchasing labs which measure our "cortisol-metabolic-activity". That way we could regulate our prednisone or medrol levels up or down, based on our how our body metabolises that prednisone or medrol, under the influence of our daily physical and mental stressors.

But none of this is possible.

Since there are no commercial labs which can measure our serum prednisone or medrol levels, therefore we have to go on symptoms only (100%).

But the symptoms of long term slightly excessive cortisol-metabolic-activity are damaged arteries, excessive internal fibrotic tissue, and a host of other mild but universally degenerated tissue states.

This is due to the fact that excess cortisol-metabolic-activity downregulates both our testosterone production, and our growth hormone production, and it also downregulates our cells' response to testosterone and growth hormone.

In short, excess cortisol-metabolic-activity downregulates our ability to trigger our body's repairs. Which is why long term excess prednisone or medrol is insidiously dangerous, if you're monitoring only symptoms alone.

Ie: the vast majority of the side effects of excess prednisone and medrol relate to the fact that our body repairs itself inadequately.

And after years of subtle gradual degeneration, the symptoms will eventually become obvious, but by then the damage is so entrenched that recovery from that point can only be partial, not complete.

###

Another interesting thing about cortisol supplementation, and prednisone or medrol supplementation, is that when there are no labs around, the person is most likely to take too much not too little.

If you take just a little "too little cortisol" (or prednisone or medrol) then it's immediately obvious, because it results in tiredness (yawning). But too much cortisol only results in "too much alertness", and in our hustle and bustle world, that's a great thing until it causes insomnia, and patients soon learn to crank up the alertness during the day, and back off at night to just below the insomnia point.

And they think (incorrectly) that this is great.

But the price of all that extra alertness during the day adds up to a lot less repairs during the day than had they optimized their cortisol levels to what their body can handle. In effect they cause their body to inadequately repair itself during the day, requiring more repairs at night than their testosterone and growth hormone levels can manage.

Obviously if they go too far, they'll cause obvious illnesses.

But the most likely scenario, is that the person will always be just a little too high in order to be able to maximise their stress tolerance - but at the price of cumulative damage which will wreak havoc in the long term.


CONCLUSION RE MEDROL AND PREDNISONE:

The long term continuous (no breaks) use, or the long term continual use (recurring use with short breaks), of prednisone or medrol, is never ever going to be good, because you cannot optimize the amount of prednisone or medrol in your body, and it's more likely that you'll take too much, over that time, than take too little.

####

Slow release cortisol is definitely the future of cortisol modulation therapy.

The cortisol molecules inserted into the body can be directly measured, which means we can use our usual labs to ensure we aren't taking too much or too little.

Of course the carrier used to encapsulate the slow release hydrocortisone may still be a molecule which is foreign to the human body, and may be just as toxic in the human body as medrol or prednisone, over the long term.

So that remains to be seen. The jury's still out on slow release cortisol.

###

But the verdict is clear on prednisone and medrol. They're foreign, there's no way to measure when they are in excess or too low other than symptoms, and the subtle long term damage from slightly excessive levels of prednisone or medrol will leave behind so much damage as to be only partially recoverable by the time the insidious and pervasive damage caused by decades of use gets discovered.

[Ozzie]

agreed that slow release cortisol is, for most, the ideal choice. Until that time comes, however, Medrol is the better choice for me. My sked is just way to hectic with all the meetings, travelling, events, etc. and with just one 4mg Medrol tab in the morning, i feel considerably better than i did with 20 mg of hydrocortisone. Moreover, it's a consistent dose and still considered sub-physiological.

Even the highly respected Thierry Hertoghe will prescribe while advising folks to monitor side-effects above 5mg which is when, in his estimation, some of the more deleterious implications start to kick in.

While metabolic activity can be measured directly, one can still glean lots of useful information from monitoring serum ACTH (you don't want to take so much as to have it ratcheted down to zero) as well as periodically taking the ACTH stim tests in order to measure progress related to Adrenal reserve.

Additionally, for me anyways, the Medrol is better given my predilection toward high BP.

I do agree with Chillin' that ultimately, natural is still better and when the slow release cortisol becomes available, i will make the switch and find other means to address my high BP.

[chilln]

Moreover, it's a consistent dose and still considered sub-physiological.


Different levels are appropriate for different people. You're attempting to apply a generalization to your specific circumstances, and it's not reliable for long term optimal health.





While metabolic activity can be measured directly, one can still glean lots of useful information from monitoring serum ACTH (you don't want to take so much as to have it ratcheted down to zero) as well as periodically taking the ACTH stim tests in order to measure progress related to Adrenal reserve.


ACTH is a pulsatile hormone. In 2009 we do not have affordable "portable continuous ACTH samplers" which we can strap on and work with during the day to monitor our pulsatile levels of ACTH.

This is not an option.

###

Your point about ACTH stimulation tests ( which help determine the adrenals capacity to manufacture cortisol in response to a hefty dose of ACTH ) is not specific to prednisone or medrol.

It can be used for cortisol and for slow release cortisol too.

Ie: this is a good option to determine whether you can turn off the prednisone or medrol or cortisol or slow release cortisol, and go back to a normal life.

But there are many other ways to determine whether you can switch off your prednisone or medrol or cortisol or slow release cortisol, eg: back off a little and see how you go.




Even the highly respected Thierry Hertoghe will prescribe while advising folks to monitor side-effects above 5mg which is when, in his estimation, some of the more deleterious implications start to kick in.


What you're saying is that Dr Thierry Hertogue can't offer anyone a lab mechanism to help monitor the metabolic effects of prednisone or medrol.





Additionally, for me anyways, the Medrol is better given my predilection toward high BP.


Medrol triggers most of the the same biological activity as cortisol, so what's keeping your blood pressure in check is the fact that the medrol dose is constant, and decays smoothly over many hours - so you're not having to dose up high, on "fast decay" hydrocortisone, in order to still have enough cortisol-metabolic-activity going on 4 hours later (which is what you had to do with hydrocortisone) and it was those fluctuating too high doses of hydrocortisone which raised your blood pressure.

Slow release cortisol will give you the same effects as medrol.




I do agree with Chillin' that ultimately, natural is still better and when the slow release cortisol becomes available, i will make the switch and find other means to address my high BP.

You won't have to find other means to address your high blood pressure.

[JanSz]

Even the highly respected Thierry Hertoghe will prescribe while advising folks to monitor side-effects above 5mg which is when, in his estimation, some of the more deleterious implications start to kick in.



There is a "consensus" that long term safe dose is;

30mgHC=6mgMedrol

one time dr John even upped to 40mgHC

If the 5mgMedrol is mentioned in dr Hertoge's book
and you know the relevant page #, please post it.
.
.

[chilln]

There is a "consensus"

Consensus doesn't validate a therapy's long term safety.

Long term safety, for an individual, is achieved via judicious decisions re supplement dosing, based on:

a) the individual's symptoms (already being done)

and

b) the individual's labs (not able to be done because direct measurements of cortisol-metabolism are not yet commercially available while supplementing with medrol or prednisone)

###

If you want to "reverse engineer" what may be an individual's cortisol-metabolism-activity, from the metrics of that person's hormones, when that person is triggering their cortisol-metabolism-activity via medrol or prednisone, then there are probably only around 5 medical professional advisers in the USA who could do that.

###

The value of the long term safe dose of 30mg HC (hydrocortisone) is definitely not generic to all males.

If we gave that much HC to some males on this forum, for several years, then they would have long term health problems for sure.

That's because different people's adrenal cortisol production shuts down to different degrees, when either medrol or prednisone are present, and this adrenal cortisol contributes to their total cortiol-metabolism-activity.

That's also because some males have slower metabolisms than others, and therefore they need less HC or medrol or prednisone than the rest of us.

###

Since the long term effects of excess prednisone or medrol are mostly due to small but omnipresent excesses in cortiol-metabolism-activity, therefore not taking into consideration the person's adrenal cortisol production contribution, or their metabolic rate of metabolism of medrol or prednisone, will result in long term effects due to too much cortiol-metabolism-activity.

[Kydd]

agreed that slow release cortisol is, for most, the ideal choice. Until that time comes, however, Medrol is the better choice for me. My sked is just way to hectic with all the meetings, travelling, events, etc. and with just one 4mg Medrol tab in the morning, i feel considerably better than i did with 20 mg of hydrocortisone. Moreover, it's a consistent dose and still considered sub-physiological.

Even the highly respected Thierry Hertoghe will prescribe while advising folks to monitor side-effects above 5mg which is when, in his estimation, some of the more deleterious implications start to kick in.

While metabolic activity can be measured directly, one can still glean lots of useful information from monitoring serum ACTH (you don't want to take so much as to have it ratcheted down to zero) as well as periodically taking the ACTH stim tests in order to measure progress related to Adrenal reserve.

Additionally, for me anyways, the Medrol is better given my predilection toward high BP.

I do agree with Chillin' that ultimately, natural is still better and when the slow release cortisol becomes available, i will make the switch and find other means to address my high BP.

If you are Secondary AI the ACTH is low/deficient before you even start any corticosteroids. So apart from the pulsatile nature of ACTH as Chillin mentions for Secondaries ACTH is suppressed to Zero or close to with very little HC/Pred/Medrol. So monitoring ACTH achieves nothing. Nor does "periodic ACTH Stims". Secondaries dont have "problems with reserves" they have lack of stimulation of the Adrenals because of low ACTH. oing off meds periodically when Secondary is just plain dangerous.

[pmgamer18]

I am secondary my Dr. tests my Cortisol levels after taking 10 mgs of Cortef in the morning as long as my labs come back showing a level. I am to him OK not over doing it. Last test come back at 12. Now when your on HC and you measure cortisol your not measuring the HC your measuring what your Adrenals are putting out.

If you are SEcondary AI the ACTH is low/deficient before you even start any corticosteroids. So apart from the pulsatile nature of ACTH as Chillin mentions for Secondaries ACTH is suppressed to Zero or close to with very little HC/Pred/Medrol. So monitoring ACTH achieves nothing. Nor does "periodic ACTH Stims". Secondaries dont have "problems with reserves" they have lack of stimulation of the Adrenals because of low ACTH. oing off meds periodically when Secondary is just plain dangerous.

[hardasnails1973]

I am secondary my Dr. tests my Cortisol levels after taking 10 mgs of Cortef in the morning as long as my labs come back showing a level. I am to him OK not over doing it. Last test come back at 12. Now when your on HC and you measure cortisol your not measuring the HC your measuring what your Adrenals are putting out.

Best sound piece of advice I have heard all day. Measure the clincal response to gauge proper treatment. I get my ass reemed out for suggesting this on thyroid boards, but one that have suggested are the ones that are improving LOL GO figure right.

[Kydd]

Prednisone and medrol are NOT bioidentical to cortisol. They are man made molecules which are similar to cortisol, but not close enough. This is why they are not metabolized as quickly as cortisol.
Never said they were bioidentical. By the way I was talking about PredNISOLONE not Prednisone.

Normally, when we want to dose a hormone modulating drug or supplement, we use both symptoms and labs, not just one or the other.
Yep normally yes. But having said that SYMPTOMS take precedence over Labs.

But neither prednisone nor medrol can be measured by a cortisol lab test. And there are no commercial prednisone or medrol lab tests available in any case.
Yes so?

If it were possible (which it is not) we would dose prednisone or medrol reliably by purchasing labs which measure our "cortisol-metabolic-activity". That way we could regulate our prednisone or medrol levels up or down, based on our how our body metabolises that prednisone or medrol, under the influence of our daily physical and mental stressors.
What happened to dosing by Labs & symptoms? Dosing by Labs only is almost a guarantee of underdosing. Just ask any Endo what they think is a "good lab result". Your proposol leaves aside a whole range of issues. Like who decides what the Lab ranges are? Who decides where in Lab range is optimal or healthy. Given that Lab ranges mean nothing as far as each INDIVIDUAL goes what should happen is you test your levels when you feel the best. Then THAT level is your individual "optimal".

Dont you all go by what I just described for your Sex Hormone replacement?
Why is Cortisol any different?

But none of this is possible. Since there are no commercial labs which can measure our serum prednisone or medrol levels, therefore we have to go on symptoms only (100%).
And I have NO problem with that at all!!!

But the symptoms of long term slightly excessive cortisol-metabolic-activity are damaged arteries, excessive internal fibrotic tissue, and a host of other mild but universally degenerated tissue states.
So? You test periodically for Blood Sugars, Cholesterols, CRP, Fibrinogen, Homocysteine, CBC, ESR, Liver & Kidney Tests, BPs & HR monitoring etc etc. Same as ANYONE whether on steroids or not should be doing!!!

This is due to the fact that cortisol-metabolic-activity downregulates both our testosterone production, and our growth hormone production, and it also downregulates our cells' response to testosterone and growth hormone.
No it doesnt unless it is in EXCESS. Normal levels do NOT. Low levels cause a myriad of health problems too. If Thyroid, Sex Hormones, Nutrition (vits, mins etc) are optimised GH & IGF-1 are often higher than when first dxed anyway even if GH HRT is never done!!!! Cortisol HRT will reduce Androgens true thats why they should be monitored & optimised. Secondaries have lousy Sex Hormone levels even before Cortisol HRT & gets even worse after.

In short, excess cortisol-metabolic-activity downregulates our ability to trigger our body's repairs. Which is why long term excess prednisone or medrol is insidiously dangerous, if you're monitoring only symptoms alone.

Ie: the vast majority of the side effects of excess prednisone and medrol relate to the fact that our body repairs itself inadequately

And after years of subtle gradual degeneration, the symptoms will eventually become obvious, but by then the damage is so entrenched that recovery from that point can only be partial, not complete..
I can agree with ony to this point. That excess Cortisol is dangerous. It makes not one iota of difference whether you take HC or Medrol or any other steroid. An excess is dangerous & a deficiency/shortfall is ALSO dangerous.

Another interesting thing about cortisol supplementation, and prednisone or medrol supplementation, is that when there are no labs around, the person is most likely to take too much not too little.
Dont agree at all.

If you take just a little "too little cortisol" (or prednisone or medrol) then it's immediately obvious, because it results in tiredness (yawning). But too much cortisol only results in "too much alertness", and in our hustle and bustle world, that's a great thing until it causes insomnia, and patients soon learn to crank up the alertness during the day, and back off at night to just below the insomnia point.And they think (incorrectly) that this is great.
Cortisol does NOT make you alert. It is calming. If you are hyped up it is more likely you have excess Adrenaline. Excess Adrenaline is often the bodies repsonse to a lack of energy. That can be due to low Cortoisol, nutritional deficiencies, low Thyroid etc.

Low Cortisol can also cause Insomnia. In fact thats one of the main symptoms my Wife had as do my kids. Cortisol HRT has improved that.

But the price of all that extra alertness during the day adds up to a lot less repairs during the day than had they optimized their cortisol levels to what their body can handle. In effect they cause their body to inadequately repair itself during the day, requiring more repairs at night than their testosterone and growth hormone levels can manage. Obviously if they go too far, they'll cause obvious illnesses.

But the most likely scenario, is that the person will always be just a little too high in order to be able to maximise their stress tolerance - but at the price of cumulative damage which will wreak havoc in the long term.
Its Thyroid & nutrition base that determines energy levels. And repair too.And good sleep & good exercise etc etc etc.

By the way how does staying on HC which requires you to dose every 2-3 hours HELP you "repair in your sleep"????


CONCLUSION RE MEDROL AND PREDNISONE:

The long term continuous (no breaks) use, or the long term continual use (recurring use with short breaks), of prednisone or medrol, is never ever going to be good, because you cannot optimize the amount of prednisone or medrol in your body, and it's more likely that you'll take too much, over that time, than take too little.
Nope disagree again. You are assuming everyone is Primary too. You cannot "take breaks". Even severe Primaries cannot "take breaks". You CAN optimise Medrol Pred in your body. I just happen to disagree with you what optimisation means.

Seems to me you are deathly afriad of Cortisol HRT in any form. In which case I advise its best you never take any in any form. But dont try & put fear in everyone elses mind.

You seem to think that Labs DO mean more than anything else. You also seem to have undying faith in measuring Cortisol when on HC which I do not share either. I know thats contrary to what some folks on this board think.
Labs on HC are just too variable to mean much of anything as far as I can see. Some folks sow very high & some very low while on HC. To dose by them instead of symptoms is just plain crazy.

Slow release cortisol is definitely the future of cortisol modulation therapy.

The cortisol molecules inserted into the body can be directly measured, which means we can use our usual labs to ensure we aren't taking too much or too little.

Of course the carrier used to encapsulate the slow release hydrocortisone may still be a molecule which is foreign to the human body, and may be just as toxic in the human body as medrol or prednisone, over the long term.

So that remains to be seen. The jury's still out on slow release cortisol.

Well you've just shot your own argument down. If bioidentical is better then once it is altered it is not bioidentical is it? So slow release anything is NOT bioidentical.

Medrol/Pred is NOT Toxic!!!! In what way are they toxic?

But the verdict is clear on prednisone and medrol. They're foreign, there's no way to measure when they are in excess or too low other than symptoms, and the subtle long term damage from slightly excessive levels of prednisone or medrol will leave behind so much damage as to be only partially recoverable by the time the insidious and pervasive damage caused by decades of use gets discovered.
No the "verdict" is NOT clear. This is scaremongering again and your opinion which I do not share. The ONLY way to "measure" Cortisol HRT is SYMPTOMS whether you are on HC or Medrol/Pred. Thats my opinion & the opinion of a great many Docs too.

Really you can go for decades being in robust health, fantastic energy, all other Labs perfect, BP & HR perfect, when all the while according to you "are being damaged inside irreversibly".

Comeon!!!!

Did someone you know have a bad Doc who damaged them through high dose Medrol/Pred? I really cannot see why you are so prejudiced against these drugs otherwise. When used in pysiological doses they are good practical alternatives for those that need them when HC does not suit for whatever reason.

[Kydd]

I am secondary my Dr. tests my Cortisol levels after taking 10 mgs of Cortef in the morning as long as my labs come back showing a level. I am to him OK not over doing it. Last test come back at 12Now when your on HC and you measure cortisol your not measuring the HC your measuring what your Adrenals are putting out.

I thought everyone here is saying you measure Cortisol while on HC in order to measure if you are on too much or too little?

If what shows up in testing is NOT HC then how is it showing whether your HC dosing is inadequate or not?

If your ACTH was suppressed (more likely if Secondary) your Adrenals wouldnt be producing anything at all would they???

Chillin posted a long post saying how dangerous Pred/Medrol was precisely because it DOESNT show up in Labs. Now you are saying neither does HC? So by Chillin's logic then HC is every bit as dangerous as Medrol and Pred too?

Are you talking about Serum testing Phil? If so how does that show anyting? Thats total Cortisol not free? We dx AI by Saliva (Free) Cortisol dont we? So why make any judgement on excess/deficient/adequate on Serum testing? I know Hertoghe uses 24 hour Urine testing which is at least Free Cortisol.

[chilln]

By the way I was talking about PredNISOLONE not Prednisone.


You are actually talking about both. Prednisolone is Prednisone.
They're different names for exactly the same molecule.

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MEDROL / PRED PRACTICAL



When used in pysiological doses they are good practical alternatives for those that need them when HC does not suit for whatever reason.


They are less-than-optimum practical alternatives, and will be superceded by SRHC (slow-release hydrocortisone), because medical professional advisers will be able to directly and accurately monitor a patient's cortisol levels using 4 x salivary cortisol labs, when the patient is supplementing with SRHC (slow-release hydrocortisone). See next topic.

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LABS VERSUS SYMPTOMS



The ONLY way to "measure" Cortisol HRT is SYMPTOMS whether you are on HC or Medrol/Pred. Thats my opinion & the opinion of a great many Docs too.


and



SYMPTOMS take precedence over Labs.


and



You seem to think that Labs DO mean more than anything else.


and



What happened to dosing by Labs & symptoms? Dosing by Labs only is almost a guarantee of underdosing.


and



You also seem to have undying faith in measuring Cortisol when on HC which I do not share either. I know thats contrary to what some folks on this board think.


and



Labs on HC are just too variable to mean much of anything as far as I can see. Some folks sow very high & some very low while on HC. To dose by them instead of symptoms is just plain crazy.



I say we should dose our HC and our Medrol/Pred using 50% labs and 50% symptoms. No more, no less.

The views that labs are less helpful than symptoms, when monitoring cortisol levels, are only the views of docs who aren't using 4 x salivary cortisol measurements. Ie: they are the views of those relying on the older technology cortisol measurements, ie: urinary cortisol and morning fasting serum cortisol.

The 4 x salivary cortisol measurements are much more accurate and reliable than urinary cortisol and morning fasting serum cortisol.

But the 4 x salivary cortisol measurements are still more expensive than the urinary cortisol and morning fasting serum cortisol, and their market penetration is still low.



Just ask any Endo what they think is a "good lab result".


Most endo's are a joke. Their mission is to help those with life threatening endocrinology conditions to get back to restore partial health (great), but they have no idea how to optimize hormones (bummer).

Here's Dr Crisler's own take on endocrinologists, it's not as flattering as your view:

http://musclechatroom.com/forum/showthread.php?t=1627


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REVERSE-ENGINEERING CORTISOL-METABOLIC-ACTIVITY






But the symptoms of long term slightly excessive cortisol-metabolic-activity are damaged arteries, excessive internal fibrotic tissue, and a host of other mild but universally degenerated tissue states.


So? You test periodically for Blood Sugars, Cholesterols, CRP, Fibrinogen, Homocysteine, CBC, ESR, Liver & Kidney Tests, BPs & HR monitoring etc etc. Same as ANYONE whether on steroids or not should be doing!!!


While medical professional advisers recommend these tests, they don't assume they can reverse engineer a person's effective-cortisol-metabolic-activity from them.

I believe you are trying to describe a situation where it is not necessary to monitor effective-cortisol-metabolic-activity, because these remaining tests suffice to determine a person's optimal health. If this is what you are attempting to do, then it is highly unreliable.

After Insulin, cortisol (or effective-cortisol-metabolic-activity) is our most critical metabolic activity. It's more important than our sex hormone activity, or our growth hormone activity, or our thyroid hormone activity.

"Effective-cortisol-metabolic-activity" cannot be reliably reverse engineered from the metrics you are suggesting.




Really you can go for decades being in robust health, fantastic energy, all other Labs perfect, BP & HR perfect, when all the while according to you "are being damaged inside irreversibly".


The vast majority of people on this forum can only afford very irregular comprehensive testing, the way you are describing. And they especially won't be able to afford regular comprehensive testing as they get older and retire.

The vast majority of people on this forum do not have a medical professional adviser who can reverse engineer their cortisol-metabolic-activity from labs other than cortisol labs.

Yet it's these older / retired people who will experience the long term debilitating effects of excess cortisol-metabolic-activity (excess Medrol/Pred), due to having monitored it via symptoms alone, because cortisol labs can't be used to assess the cortisol-metabolic-activity of Medrol/Pred.





No it doesnt unless it is in EXCESS.


I stand corrected, but I meant excess, and I included the "excess" word the very next time I mentioned the term cortisol-metabolic-activity.




I can agree with ony to this point. That excess Cortisol is dangerous. It makes not one iota of difference whether you take HC or Medrol or any other steroid. An excess is dangerous & a deficiency/shortfall is ALSO dangerous.


The fact value statement would be correct, if only the underlying assumption were not flawed. But the underlying assumption is flawed.

Underlying this statement is one of two assumptions:
.....a) that a person's medical professional adviser can reliably determine excess cortisol-metabolic-activity of Medrol/Pred via symptoms alone,
or
.....b) that a person's medical professional adviser never needs to determine a patient's cortisol-metabolic-activity.

We and our medical professional advisers have long ago established that we need to measure cortisol levels when we supplement with SRHC (slow-release hydrocortisone) because we can compare those supplementary cortisol levels on a one-for-one basis with our "unassisted" optimal adrenal-produced-cortisol levels, and they should be the same under similar body-stress conditions.

Our medical professional advisers know that we all need those labs to either:
.....a) corroborate symptoms,
or
.....b) contradict symptoms - in which case there may be alternative hormone dysfunctions which explain the symptoms.

But there are no labs which directly measure cortisol-metabolic-activity for Medrol/Pred.

Which means we are at risk of supplementing with excess Medrol/Pred more so than we are at risk of supplementing with excess SRHC (slow-release hydrocortisone).

###

I accept that the reliability of measuring cortisol via urinary or morning fasting serum cortisol was less-than-optimum, but we now have more accurate cortisol testing in the form of 4 x salivary cortisol testing.

So the reliability of cortisol labs (ie: salivary 4 x cortisol) is on par with the reliability of monitoring symptoms.


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MISCELLANEOUS




Cortisol does NOT make you alert.


I specifically commented about excess cortisol, and insufficient cortisol.

Since you omitted the word "excess" or "insufficient" therefore I have to assume you mean all of :
a) insufficient Cortisol does NOT make you alert.
and
b) optimum Cortisol does NOT make you alert.
and
c) excess Cortisol does NOT make you alert.

That's silly.




Low Cortisol can also cause Insomnia. In fact thats one of the main symptoms my Wife had as do my kids. Cortisol HRT has improved that.


I agree that low cortisol can cause insomnia.

Excess cortisol-metabolic-activity, at night, also causes insomnia.




Its Thyroid & nutrition base that determines energy levels. And repair too.And good sleep & good exercise etc etc etc.


Insufficient cortisol results in constant fatigue.

Even though cortisol isn't a direct player in the ATP/ADP energy cycle, it's still a critical prerequisite.




By the way how does staying on HC which requires you to dose every 2-3 hours HELP you "repair in your sleep"????


I never once stated that it did.

I am not arguing the case that HC supplementation is optimum, I am arguing the case that SRHC (slow-release hydrocortisone) will be better than Medrol/Pred.


cont'd next post...

[chilln]

...cont'd from previous






Slow release cortisol is definitely the future of cortisol modulation therapy.

The cortisol molecules inserted into the body can be directly measured, which means we can use our usual labs to ensure we aren't taking too much or too little.

Of course the carrier used to encapsulate the slow release hydrocortisone may still be a molecule which is foreign to the human body, and may be just as toxic in the human body as medrol or prednisone, over the long term.

So that remains to be seen. The jury's still out on slow release cortisol.



Well you've just shot your own argument down. If bioidentical is better then once it is altered it is not bioidentical is it? So slow release anything is NOT bioidentical.


Even if the first generation of slow-release-cortisol is not the best ever, that doesn't mean the future of slow-release-cortisol is something else (eg: Medrol/Pred).

That only means the future of cortisol supplementation (or cortisol-like molecule supplementation) will be delayed until the second or maybe third generation of slow-release-hydrocortisone.

That's because once the hydrocortisone is released from its carrier, it is measurable via labs, and that's exactly why the pharma company is developing a mechanism to encapsulate HC.

But the future of cortisol supplementation (or cortisol-like molecule supplementation) is not Medrol/Pred.

That's because we cannot directly measure the cortisol-metabolic-activity of Medrol/Pred, and there are far too few people on this planet who can reverse engineer the cortisol-metabolic-activity of these molecules.

But medical professional advisers will be able to directly and accurately monitor a patient's cortisol levels using 4 x salivary cortisol labs, when the patient is supplementing with SRHC (slow-release hydrocortisone).









The long term continuous (no breaks) use, or the long term continual use (recurring use with short breaks), of prednisone or medrol, is never ever going to be good, because you cannot optimize the amount of prednisone or medrol in your body, and it's more likely that you'll take too much, over that time, than take too little.


Nope disagree again. You are assuming everyone is Primary too.


I don't assume everyone is primary. I'm addressing people who use Medrol/Pred either continuously or continually.

Only you are assuming that everyone who uses Medrol/Pred is primary.

Some of those people are primary, some are secondary.

The ones who are secondary, and who use Medrol/Pred either continuously or continually, are the ones who either:
.....a) are not aware their T (testosterone) and/or GH (growth hormone) have tanked, and must address a permanent state of adrenal fatigue
.....b) are aware that their T and/or G have tanked, yet refuse to boost either their T or their GH, and must address a permanent state of adrenal fatigue.




Seems to me you are deathly afriad of Cortisol HRT in any form. In which case I advise its best you never take any in any form.


You're playing the man, not the ball. Please stay on topic.




But dont try & put fear in everyone elses mind.


If you suspect I am attempting to subject people to fear, then that's your view, so be it. It's not my view. I don't care much for emotion, and I don't waste my time attempting to educate adults via emotional means.

I do use emotional means to educate children, but there are no children on this forum.




Medrol/Pred is NOT Toxic!!!! In what way are they toxic?


The definition of toxicity is not "deadly". The definition of toxic is "debilitating for health". It's anything from a little bit of a problem, to a lot of a problem.

Medrol/Pred exhibit toxicity in two ways:

1) By stealth.

Since we cannot reliably determine when excess levels of Medrol/Pred have been achieved from symptoms alone, therefore there will be a proportion of users of Medrol/Pred who are taking excess Medrol/Pred, and who assume they are fine. But had they been able to validate their cortisol-metabolism-activity via direct measurement of, they would have reduced their dose appropriately.

Users of SRHC (slow-release hydrocortisone) will be able to monitor their cortisol levels and associate those with optimal natural cortisol levels, and this additional monitoring will reduce the incidence of excess SRHC (slow-release hydrocortisone), compared to the incidence of excess Medrol/Pred.


2) By bypassing one of the body's principal mechanisms for cortisol-metabolism-activity management: ACTH modulation of cortisol levels.

This mechanism is not specific to Medrol/Pred, it will also apply to SRHC (slow-release hydrocortisone).

When we make something difficult to metabolize, we remove our body's ability to optimize levels quickly. Hence the person is in charge of optimizing his/her own levels. Yet at the same time, the person only has symptoms at his disposal to optimize those levels, no labs. And judging by the feedback of forum members here, their ability to specifically associate symptoms with specific hormones, is poor.

I am aware that this mechanism also holds true the slow-release-hydrocortsone, but the difference is that medical professional advisers will be able to directly and accurately monitor a patient's cortisol levels using 4 x salivary cortisol labs, when the patient is supplementing with SRHC (slow-release hydrocortisone).






But the verdict is clear on prednisone and medrol. They're foreign, there's no way to measure when they are in excess or too low other than symptoms, and the subtle long term damage from slightly excessive levels of prednisone or medrol will leave behind so much damage as to be only partially recoverable by the time the insidious and pervasive damage caused by decades of use gets discovered.


No the "verdict" is NOT clear.


Only to you.



Did someone you know have a bad Doc who damaged them through high dose Medrol/Pred? I really cannot see why you are so prejudiced against these drugs otherwise.


You're playing the man, and not the ball. Please stay on topic.

[pmgamer18]

Good question first let me say if you want to know if your Adrenals are bad you don't take anything Glands or HC when testing. Then when your on HC and you do a blood test if your on to much your test Cortisol that is will come back suppressed not showing much at all. I tested 3 different tests to figure out I am Secondary because one is Secondary does not mean they don't make Cortisol just that they don't make enough of it. So doing labs on HC if you show a number that is low but still above the bottom of the range your not shutting down your Adrenals on to much HC. I tested between 8 to 12 on HC I still test between 8 to 12 so I am not suppressed. Simple as that this is how my Dr. told it to me and if you read Dr. Jefferies book "Safe Uses of Cortisol" he dose the same thing when treating one with HC.

I thought everyone here is saying you measure Cortisol while on HC in order to measure if you are on too much or too little?

If what shows up in testing is NOT HC then how is it showing whether your HC dosing is inadequate or not?

If your ACTH was suppressed (more likely if Secondary) your Adrenals wouldnt be producing anything at all would they???

Chillin posted a long post saying how dangerous Pred/Medrol was precisely because it DOESNT show up in Labs. Now you are saying neither does HC? So by Chillin's logic then HC is every bit as dangerous as Medrol and Pred too?

Are you talking about Serum testing Phil? If so how does that show anyting? Thats total Cortisol not free? We dx AI by Saliva (Free) Cortisol dont we? So why make any judgement on excess/deficient/adequate on Serum testing? I know Hertoghe uses 24 hour Urine testing which is at least Free Cortisol.

[JanSz]

Good question first let me say if you want to know if your Adrenals are bad you don't take anything Glands or HC when testing. Then when your on HC and you do a blood test if your on to much your test Cortisol that is will come back suppressed not showing much at all. I tested 3 different tests to figure out I am Secondary because one is Secondary does not mean they don't make Cortisol just that they don't make enough of it. So doing labs on HC if you show a number that is low but still above the bottom of the range your not shutting down your Adrenals on to much HC. I tested between 8 to 12 on HC I still test between 8 to 12 so I am not suppressed. Simple as that this is how my Dr. told it to me and if you read Dr. Jefferies book "Safe Uses of Cortisol" he dose the same thing when treating one with HC.

Phil;

chilln spelled clearly his opinion about Medrol (do not use it).

What opinion about Medrol have people on STTM?

I would rather stay the way I am now and not be scared or worried

I am feeling Much better since I switched from HC to Medrol.
Much more even and steady.
I started with 6mgMedrol=4mg/wakeup + 2mg/6-8 hrs latter
Couple times I forgot my afternoon dose and recall about it so late that I was on 4mg that whole day.
Now I am doing it on a purpose.
Last three days in the row I feel even and good on 4mgMedrol/wakeup
better than on 10+10+5+5=30mgHC

.

[pmgamer18]

If I was like the people I talked to at STTM eating up the Cortef as fast as I took it I would have went on Medrol a long time a go. It's about treatment if one dose not work why suffer do the other. I am not like them but I know people on Medrol for yrs never a problem. Every med you get comes with a long list of sides some only one person had that side effect. I can't tell you what to do but if I eat up the HC as fast the the people I have talked to I would be on Medrol.

I would not go on it because someone said they think it's better you don't do Medrol unless the HC your doing is not lasting.

Here is a link to what one person says about taking it.
http://www.geocities.com/chrisgj@sbcglobal.net/My_explanation_when_switch_HC_Cortef_to_Medrol.htm l

Still I don't do anything without my Dr.

Phil;

chilln spelled clearly his opinion about Medrol (do not use it).

What opinion about Medrol have people on STTM?

I would rather stay the way I am now and not be scared or worried

I am feeling Much better since I switched from HC to Medrol.
Much more even and steady.
I started with 6mgMedrol=4mg/wakeup + 2mg/6-8 hrs latter
Couple times I forgot my afternoon dose and recall about it so late that I was on 4mg that whole day.
Now I am doing it on a purpose.
Last three days in the row I feel even and good on 4mgMedrol/wakeup
better than on 10+10+5+5=30mgHC

.

[chilln]

Phil;

chilln spelled clearly his opinion about Medrol (do not use it).


I never recommend anyone should take or not take a prescription supplement (controlled substance).

I only ever recommend discussion topics which you should have with your medical professional adviser.

That's why I always include the following phrase "discuss with your medical professional adviser to boost your..."

###

In case the generic concept is not self-evident, I'll apply it specifically to Medrol/Pred:

I have never said "don't take Medrol/Pred", because that also constitutes medical advice,
...and
I have provided information re the potential long term effects of Medrol/Pred, which you should discuss with your medical professional adviser.

Your medical professional adviser will let you know whether you should take Medrol/Pred.

###

Finally, my discussions have avoided comparisons between Medrol/Pred and the current generation of immediate-release hydrocortisone (HC / Cortef).

The only statement I have made which specifically addresses a comparison between Medrol/Pred and immediate-release HC is the following:





When used in pysiological doses they are good practical alternatives for those that need them when HC does not suit for whatever reason.


They are less-than-optimum practical alternatives, and will be superceded by SRHC (slow-release hydrocortisone), because medical professional advisers will be able to directly and accurately monitor a patient's cortisol levels using 4 x salivary cortisol labs, when the patient is supplementing with SRHC (slow-release hydrocortisone).

[JanSz]

I never recommend anyone should take or not take a prescription supplement (controlled substance).

I only ever recommend discussion topics which you should have with your medical professional adviser.

That's why I always include the following phrase "discuss with your medical professional adviser to boost your..."

###

In case the generic concept is not self-evident, I'll apply it specifically to Medrol/Pred:

I have never said "don't take Medrol/Pred", because that also constitutes medical advice,
...and
I have provided information re the potential long term effects of Medrol/Pred, which you should discuss with your medical professional adviser.

Your medical professional adviser will let you know whether you should take Medrol/Pred.

###

Finally, my discussions have avoided comparisons between Medrol/Pred and the current generation of immediate-release hydrocortisone (HC / Cortef).

The only statement I have made which specifically addresses a comparison between Medrol/Pred and immediate-release HC is the following:

Your discussion of pro and con of Hydrocortisone vs Medrol/Pred
are very insightful and valuable, thank you.

Same with discussing hormone pathways and other health situations.

When my Cortef was running out, my medical advisor had no problem writing script for Medrol. Minimal/no discussion.

Q----Doc, my Cortef is wearing out before there is a time for the next dose, may I try Medrol.
A---Yes.

=============================================
Asking for medical advice is similar to many life situations,
it helps to know 3/4 of an answer to the question one asks.
------------
Thank you for providing so many usefull informations.
.

[JanSz]

http://musclechatroom.com/forum/showpost.php?p=52022&postcount=6


I take 87.5 mcg of cytomel T3 each morning. You are better off on cytomel. SRT3 (sustained release T3) is not predictable because there are several substances in foods that block absorption. For that reason it is always advised that T3 is taken on an empty stomach. People have the misconception that T3 is very fast acting and it needs to be spread out. This misconception stems from the fact T3 blood levels peak within a couple hours of consumption. What is not accounted for is the "buffering effect" of the "genomic" actions of T3:

I’ve found that some patients have markedly improved or recovered with the use of timed-release T3. I assume that most of these patients were hypothyroid. However, I’ve also found that many patients either don’t benefit with timed-released T3, or they improve only slightly. When we switch these patients to plain T3, most have markedly improved or completely recovered. (Of course, the use of thyroid hormone isn’t the only component of our patients’ regimen. We require that all patients engage in a more comprehensive regimen of metabolic rehab. So, when I refer to a patient improving under our care, invariably, the patient has also engaged in other metabolism-regulation methods. Such methods include diet modifications, nutritional supplementation, and exercise to tolerance.)

I suspect that the reason most patients don’t have inconsistent physiological responses to plain T3 is a "buffering effect" of the "genomic" actions of T3. Most effects of T3 on the body are not a result of direct actions of the hormone on cells. Instead, most effects of T3 result from the actions of the hormone on genes in cell nuclei. These genomic actions of T3 appear to serve as a "buffer." By this I mean that most cells are protected from a direct, abrupt effect of T3. The physiologic effects of T3 are highly indirect. The effects result from changes in protein synthesis due to T3-induced alterations in gene transcription.

When a patient takes T3, the hormone must first enter the cells and then enter their nuclei. Next, the hormone must bind to T3-receptors on different genes. The binding of T3 to T3-receptors on genes alters the genes’ transcriptional activity. Transcription of some genes is activated; that of others is inhibited. The resulting increase in messenger RNA from the activation of genes may also be enhanced by post-transcriptional actions of T3. For example, T3 may increase the survival time of some messenger RNAs. The increase or decrease in gene transcription (resulting from the transcription-regulating effects of T3/T3-receptor binding on genes) changes the numbers of proteins synthesized by cells. The change in concentrations of the proteins then alters physiology. For instance, the concentration of the apoenzyme component of various enzymes is increased. The increase in the concentration of the enzymes then alters the rate of different biochemical reactions, and this is reflected in changed physiology.

http://www.drlowe.com/jcl/comentry/t3instablility.htm

=========================
http://www.lef.org/magazine/mag2009/jun2009_Using-Blood-Test-Findings-To-Induce-Weight-Loss_03.htm

"For optimal fat-loss effects, a person may be prescribed small doses of Cytomel® (a prescription form of T3) if their T3 levels are not in the upper one-third range of normal, or if consuming fewer calories results in a reduction of T3 levels."

=========================
http://musclechatroom.com/forum/showpost.php?p=52062&postcount=8

First people were cursing life on Synthroid(T4)
Armour was a big improvement over plain T4
That is because of its 20% of T3 content

But many people need more T3 than is contained in Armour.

T3 is not recognized yet but it is coming.

Only in July/09 LEF magazine
I see first writings that we need much more T3

---------------------
===========================
===========================
http://musclechatroom.com/forum/showpost.php?p=52078&postcount=11


You are right Jan. The reason that T4 doesn't work for most and why Armour does not work for many is the T4 component. T4 very quickly reduces TSH and if you are not converting it properly it is even worse. Your body goes hypo which can slow down it's already impaired ability to convert T4 even further. T3 is the answer here. There is no relying on anything else. T3 is the active form. It works 100% and there is no guessing about conversion or any other nonsense.

It is also much, much easier to regulate because of it's shorter 1/2 life. If you take too much you can correct your overstimulated or condition with in hours to a couple days. It makes it much easier to adjust than the weeks you have to wait when using a t4 containing product.

I have had excellent success with T3. Where T4 made me weak, dizzy and sick. T3 made me feel great. My testosterone went from 200's to 700 within a month when I got to my full dose and my metabolism was finally properly regulated.

I think many people get shafted by doctors using t4 or armour that go by labs instead of using t3 and measuring metabolism. I am sure there are lots of guys out there who are on TRT because they have not gotten enough T3 to regulate their perfectly fine working gonads.

[JanSz]

http://www.questdiagnostics.com/hcp/intguide/jsp/showintguidepage.jsp?fn=CF_Osteo.htm

Thyrotoxicosis

Thyroid hormone excess leads to increased bone resorption. A low TSH level, along with high free T4 and free T3 levels, suggests thyrotoxicosis. Alkaline phosphatase and serum calcium levels may be elevated.

.

[JanSz]

-------http://www.scribd.com/doc/1959949/IODINE-Solution-to-Healthproblems

page 38/95

Iodine is detoxifying agent

detoxifies the other Halides,
bromine, fluoride, chlorine

detoxifies toxic metals
mercury, lead, aluminum, cadmium
----------------------------------------------

not sure I think, iodone depletes vit E, A, may require extra supplementation
(page 49)
.
.
.

[JanSz]

-------------------------------------------------------------------------
http://www.privatemdlabs.com/lab_tests.php?view=all&show=1250&category=11&search=#1250
------------------------------------------------------------------------
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Hematocrit; hemoglobin; Cholesterol, albumin, glucose, potassium, sodium (many others)

- Complete Blood Count w/ Differential
- Lipid Profile
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- Serum Iron
- Complete Urinalysis Profile
- Serum Electrolytes
-------------------------------------------------------------
Iron, Comprehensive Panel $54.49
Includes: Iron, serum; Ferritin, serum; total iron binding capacity (TIBC);
-------------------------------------------------------------
Cortisol Serum AM & PM $149.49
-------
Renin Activity and Aldosterone $98.99
-----------------------------------------
Thyroid Antibodies $98.49
Thyroid Profile II (Comprehensive) $88.49
Free thyroxine index (FTI); T3 uptake (THBR); thyroid-stimulating hormone (TSH); thyroxine (T4); tri-iodothyronine (T3).
-----------------------------------------
Thyroid TSH w/ Free T4 & Free T3 $78.49
-----------------------------------------
Testosterone, Total, Serum $44.49
Sex Hormone binding Globulin, Serum $49.49
Estradiol, Sensitive $68.49
Dihydrotestosterone (DHT) $119.99
-----------------------------------------------------------------------------

.......

[EIC]

Earlier in this thread it was mentioned that one could ensure proper T4 --> T3 conversion by ensuring adequate . . .

1) Cortisol (presumptively through HC)
2) Iodine (via Lugol's or Iodoral)
3) Selenium
4) Zinc
5) Iron

I may have missed some.

My question concerns selenium: Is there a minimum amount that one should consider supplementing with to ensure proper T4 --> T3? It looks like standard doses are in the 200 mcg. range.

This is a subject I have much interest in at the moment seeing as how I am currently limited to Levothyroxine.

[JanSz]

Earlier in this thread it was mentioned that one could ensure proper T4 --> T3 conversion by ensuring adequate . . .

1) Cortisol (presumptively through HC)
2) Iodine (via Lugol's or Iodoral)
3) Selenium
4) Zinc
5) Iron

I may have missed some.

My question concerns selenium: Is there a minimum amount that one should consider supplementing with to ensure proper T4 --> T3? It looks like standard doses are in the 200 mcg. range.

This is a subject I have much interest in at the moment seeing as how I am currently limited to Levothyroxine.
It is good idea to measure first and then support missing items with proper supplementation.

If you are missing T3 and supply T4 but not able to convert it to T3 then you will have to make change.

There was a A4M presentation where Pramod Vora was working on figuring out optimal levels of select indicarors.
I have made summary of that presentation here:

http://musclechatroom.com/forum/showpost.php?p=48353&postcount=26

.

[EIC]

It is good idea to measure first and then support missing items with proper supplementation.

If you are missing T3 and supply T4 but not able to convert it to T3 then you will have to make change.

There was a A4M presentation where Pramod Vora was working on figuring out optimal levels of select indicarors.
I have made summary of that presentation here:

http://musclechatroom.com/forum/showpost.php?p=48353&postcount=26

.

Wow, Jan. That table is definitely a keeper. Glad I asked. What do the notes in the table pertain to? Are those pertinent to you specifically?

[JanSz]

Wow, Jan. That table is definitely a keeper. Glad I asked. What do the notes in the table pertain to? Are those pertinent to you specifically?

What notes?

There are two columns of values "Optimum" and "Standard"
some valueas are broken for males and females.


.

[EIC]

What notes?

There are two columns of values "Optimum" and "Standard"
some valueas are broken for males and females.


.

For example, on the left side where it says, "Abdominal Distention" then lists stomach acid, bile, enzymes, and says "Cannot be corrected by any amount of exercise."

[JanSz]

For example, on the left side where it says, "Abdominal Distention" then lists stomach acid, bile, enzymes, and says "Cannot be corrected by any amount of exercise."

Problem=Abdominal Distention

Reasons for Abdominal Distention= Improper Digestion

Problem=Improper Digestion

Reasons for Improper Digestion
a) Gastric Acids
b) Liver - bile
c) Pancreatic Enzymes


and so on


+ Enlarged and/or Fatty liver

+ Chronic constipation

Cannot be corrected by any amount of gym work

[era]

http://www.armourthyroid.com/con_faqs.aspx#q4

The basic "rule of thumb" in converting thyroid doses is that
100 mcg of T4 is roughly equal to 25 mcg of T3, or 1 grain (60 mg) of Armour Thyroid.

Endocrinology Articles
http://emedicine.medscape.com/endocrinology

I realize that some endos (e.g. Ridha Arem) use this T4:T3 = 4:1 equivalency. However it seems to diverge from my experience. (Which is somewhat unusual, because I am a recovering celiac. I suspect I had high D3 and rT3.)

When I was on T4-only last year at 118mcg (and not feeling at all well), I had a TSH<0.015. I have now been on T3-only for about 9 months. I have titrated my dose based on symptoms, and now have FT3~=4.0 , TSH<0.015, at 57.5mcg T3 (Cytomel) daily. My body mass is about 74kg, which equates to a Synthroid full replacement dose of about 126mcg.

57.5mcg T3 per day is low, compared to what is quoted by Dr. Lowe, and what is used by most people on the rt3_t3 list. Their conventional wisdom is that T3 doses in the 75-125mcg range are needed to stay un-hypo. Lowe claims he needs 150mcg/day.

Based on my experience, then, T4:T3 ratio of 2:1 (based on what works for either all T4, or all T3) seems to be how my body operates.

Of course, it could be that a 2:1 ratio reflects disorder of the D1 and D3 enzymes. Thoughts?

[JanSz]

I realize that some endos (e.g. Ridha Arem) use this T4:T3 = 4:1 equivalency. However it seems to diverge from my experience. (Which is somewhat unusual, because I am a recovering celiac. I suspect I had high D3 and rT3.)

When I was on T4-only last year at 118mcg (and not feeling at all well), I had a TSH<0.015. I have now been on T3-only for about 9 months. I have titrated my dose based on symptoms, and now have FT3~=4.0 , TSH<0.015, at 57.5mcg T3 (Cytomel) daily. My body mass is about 74kg, which equates to a Synthroid full replacement dose of about 126mcg.

57.5mcg T3 per day is low, compared to what is quoted by Dr. Lowe, and what is used by most people on the rt3_t3 list. Their conventional wisdom is that T3 doses in the 75-125mcg range are needed to stay un-hypo. Lowe claims he needs 150mcg/day.

Based on my experience, then, T4:T3 ratio of 2:1 (based on what works for either all T4, or all T3) seems to be how my body operates.

Of course, it could be that a 2:1 ratio reflects disorder of the D1 and D3 enzymes. Thoughts?

Cytomel-T3 dose up to 25-75mcg may be titrated by feel and symptoms.
After that nothing beats god tests.

..

[canthavetoomanytoys]

http://thyroid.about.com/od/loseweightsuccessfully/a/weight-loss-diet.htm

[00slotiv]

http://thyroid.about.com/od/loseweightsuccessfully/a/weight-loss-diet.htm

Another mention of time release T3 being the optimal method for T3.

Bob

[JanSz]

Another mention of time release T3 being the optimal method for T3.

Bob

I am using two 25mcg Cytomel/day (generic not original)
Also two 2mg Medrol/day (original Medrol)

I take all 4 pills after wakeup together with my morning handful of supplements and with my shots (EOD).
I try to make it as a one little project.
Next handful of supplements sometime late afternoon, and I am done with medicines and supplementing for the day.

Measure my temperatures throughout the day, always within good range.

I have a script in hand for my next blood test.
I will do a draw sometimes Nov-Dec.

....

[00slotiv]

I am using two 25mcg Cytomel/day (generic not original)
Also two 2mg Medrol/day (original Medrol)

I take all 4 pills after wakeup together with my morning handful of supplements and with my shots (EOD).
I try to make it as a one little project.
Next handful of supplements sometime late afternoon, and I am done with medicines and supplementing for the day.

Measure my temperatures throughout the day, always within good range.

I have a script in hand for my next blood test.
I will do a draw sometimes Nov-Dec.

....

I am all for Cytomel. My free T3 is on the bottom of the range now. The small amount of compounded T3 did nothing at all.

I will press again for it tomorrow.

Bob

[Wise Guy]

Bump

[JanSz]

http://musclechatroom.com/forum/showthread.php?p=56578#post56578

Hyperthyroidism unmasked several years after the medical and radiosurgical treatment of an invasive macroprolactinoma inducing hypopituitarism: a case report.

Cases J. 2009;2:6449

Authors: Foppiani L, Ruelle A, Cavazzani P, Del Monte P

INTRODUCTION: Measuring thyroid stimulating hormone levels alone may be insufficient to appropriately evaluate thyroid function. Reduced thyroid stimulating hormone levels associated to normal/reduced FT4 levels should prompt investigation of pituitary function, on suspicion of hypopituitarism. Pituitary macroadenomas are the most common cause of hypopituitarism; among these, macroprolactinomas are usually treated with dopamine-agonist therapy. Hypopituitarism does not preclude the development of primary hyperthyroidism. This report describes the case of a patient with a final diagnosis of macroprolactinoma inducing hypopituitarism, who subsequently developed hyperthyroidism due to a toxic thyroid nodule. CASE PRESENTATION: A 62-year-old man underwent biochemistry and thyroid function assessment for asthenia. Reduced thyroid stimulating hormone levels were associated to slightly decreased FT4 levels and low-normal FT3 levels; thyroid ultrasonography showed a multinodular goiter. Thyroid scan with (99m)Tc-pertechnetate revealed an autonomous left nodule with suppression of the surrounding parenchyma. Pituitary investigation showed partial hypopituitarism associated to increased prolactin levels: 182-200 ng/ml. Magnetic resonance imaging revealed a large (2.2 cm) invasive macroadenoma. To avoid a possible high-dose hook effect, the patient's serum was diluted; the resulting PRL levels of around 1800 ng/ml prompted the final diagnosis of macroprolactinoma. Reduced libido and erectile dysfunction were ascertained. In addition to replacement therapy with L-thyroxine and testosterone, cabergoline was started and was progressively increased to high doses (4 g/week); this yielded a significant but incomplete reduction of PRL levels (63-99 ng/ml). Sexual function improved. The macroadenoma shrank over the first two years of therapy, but subsequently enlarged slightly. Following stereotactic radiosurgery, the tumor stabilized and prolactin almost normalized (22 ng/ml) on therapy. Over the years, thyroid nodule volume was unmodified, but hyperthyroidism on L-thyroxine therapy was found, and increased FT3 levels with suppressed thyroid stimulating hormone levels were confirmed off-therapy. Thyroid scan confirmed the left autonomous nodule, which was successfully treated with methimazole. CONCLUSION: Reduced thyroid stimulating hormone levels associated to normal/reduced free-thyroid hormone levels may be the first clue to unsuspected hypopituitarism. Moderately increased prolactin levels in the presence of a large macroadenoma warrant serum dilution in order to avoid a possible hook effect. Stereotactic radiosurgery is a useful non-invasive tool in the management of pituitary tumors. A pre-toxic thyroid nodule with low secretory activity may initially be masked by the coexistence of secondary hypothyroidism, but may lead to overt hyperthyroidism over time.


.

[CowboyBob]

Here is a 30-minute Denis Wilson speech at A4M Orlando 2009 titled "The Use of T3 and Herbal Medicine to Reset Body Temperature and Recalibrate Many Bodily Functions":

http://www.prolibraries.com/a4m/?select=session&sessionID=2008

The 1st 3 minutes are free, then you have to register and pay to see the rest.


work on D1 enzyme and RT3 will take care of itself. no?

Dr. John concurred with this statement. What is D1? And do you want D1 levels to go up or down?


Finally.

I think I've found the best solution - and this guy is a medical professional - a pharmacist - in Australia (of all places)

http://www.custommedicine.com.au/blog/2007/04/17/reverse-t3-dominance/



The Australian site says to begin by taking 10mcg T3 SR daily, and that doses above 15mcg daily should not be used to avoid endogenous suppression. Is it safe to take 10mcg T3 SR daily? And can you only get this from a compounding pharmacy?

[00slotiv]

Here is a 30-minute Denis Wilson speech at A4M Orlando 2009 titled "The Use of T3 and Herbal Medicine to Reset Body Temperature and Recalibrate Many Bodily Functions":

http://www.prolibraries.com/a4m/?select=session&sessionID=2008

The 1st 3 minutes are free, then you have to register and pay to see the rest.



Dr. John concurred with this statement. What is D1? And do you want D1 levels to go up or down?



The Australian site says to begin by taking 10mcg T3 SR daily, and that doses above 15mcg daily should not be used to avoid endogenous suppression. Is it safe to take 10mcg T3 SR daily? And can you only get this from a compounding pharmacy?

Yes, compouning pharmacy for SR T3. Nine mcg dropped me to the very depths of the range so I will be testing the result of 27 mcg SR in about three weeks.

I have read that any amount of T3 will cause suppression and that suppression can be avoided so I am confused about that part. And what if higher amounts are needed to raise free T3 and lower reverse T3? Is that bad?

Bob

[JanSz]

http://musclechatroom.com/forum/showpost.php?p=61509&postcount=31

Re: BMR testing (tissue status testing) not really necessary

I think you have petty high standards of a 'morsel of substance'.
--------------
I take 87.5 when I wake up each morning. It lasts me through the day.

The mistake people make is thinking that bc cytomel peaks in the blood within a few hours that its action peaks the same way. Not true.

-------------------

BMR is the gold standard of metabolism measurment. With that said, I have never had my BMR measured. For me cardiac tissue is very telliing. I took basal pulse rates, resting pulses, blood pressue, blood sugar, and temperature measurements to figure out how my tissues responded. In the protocol they also use EKG's and trigger points (that access muscle sensitivity). I have noticed that my muscles are much looser than before. My necessity to stretch is much less and my visits to the chiropractor are fewer and further between.

Would I like to have my BMR, my before and after EKG's, my achillies reflex, trigger points, tested evaluated, plotted, charted and tracked? Sure, I would love to. Problem is that I have a wife, kids, a business to run, bills etc. For me it was the most feasible to get the book learn the theories and present them to my "medical professional adviser". Which is what I did.

So, I got my "morsel, thank you (JS)
------------------------------------

As I have explained, many hormones in my labs have resolved as have almost all of my symptoms. That is really the motivation of my posts. Most people when they feel fine, they just drop off the forums and they never give any other their experience back. That that is not me.

Thank you. (JS)
------------------------------------
So I am here to tell my story. It took me a couple years to figure it out. Now I am hoping that I can at least influence other people enough to be open minded to look into historicaly proven techniques of diagnosing and managing thyroid so they don't have to go the same road I had to.


Thank you. (JS)
-------------------------------------
Your welcome

....

Same.

Nice post, with a lots of "morsels' in it.

If you do not mind I will also add this post to my rt3 thread here:

post #145
http://musclechatroom.com/forum/showpost.php?p=61508&postcount=145

[JanSz]

Nice tidbit from LowT, thank you.

http://musclechatroom.com/forum/showthread.php?t=5350
---------------------------------------

http://www.csrf.net/dr_answers/question:_does_a_24-hour_urinary_cortisol_measurement_give_any_informa tion.php

Question: Does a 24-hour urinary cortisol measurement give any information on whether a patient without any adrenal glands is taking the correct amount of replacement hydrocortisone? Are there other tests that can be used to determine the correct replacement dose?

Answer: For the most part, adequacy of the hydrocortisone (glucocorticoid) dose is judged by clinical features. For example, weight gain and the development of Cushingoid features suggests that the dose is too high, while weight loss and adrenal insufficiency symptoms (joint aches, nausea), suggests that the dose is too low.

The 24-hour urine free cortisol concentration (UFC) may provide a very gross and imprecise sense of the adequacy of replacement hydrocortisone. In healthy individuals, UFC reflects the integrated blood cortisol levels during the day, and the two values correlate well. However, in the setting of hydrocortisone therapy, the relationship between blood and urine values do not always correlate well. This is explained by the way in which cortisol is carried in the blood. Only a small amount is "free" while nearly all is bound to a carrier protein. Usually the amount of cortisol in the blood can be accommodated by the carrier proteins and the appropriate amount is free. This free fraction is the part that is excreted in urine and that is available to the cells to exert hormonal effects. When a person takes a large dose of hydrocortisone, the resulting blood concentrations of cortisol may exceed the ability of the binding proteins to carry it, and the large "free" fraction is excreted in the urine. If this occurs the amount of cortisol in the urine will reflect more the "free" fraction that was excreted, rather than the "free" fraction that was available to the cells in the body. As a result, the UFC may overestimate the amount of cortisol actually available, and falsely suggest that the hydrocortisone dose is too high. This occurs most often when hydrocortisone is given as a single daily dose. On the other hand, a low UFC does not necessarily mean that the hydrocortisone dose is too low, as normal individuals may have UFC values in the lower normal range.

The question mentions a patient without adrenal glands. In general, all such patients also require a mineralocorticoid supplement, given as fludrocortisone (Florinef®). --------------------------- continued

------------------
Editor's Note: Dr. Nieman is Senior Investigator, PREB, NICHD, Deputy Branch Chief, PREB, NICHD, and Associate Director, IETP, NICHD-NIDDK at the National Institute of Health in Bethesda, MD.

.......

[JanSz]

Nice summary, Bob.
Thank you.


Comparison of T3 protocols from Denis Wilson, John Lowe, etc.

http://musclechatroom.com/forum/showthread.php?p=65009#post65009


A. BACKGROUND

All T3 protocols are for managing levels of the following Thyroid hormones: T4, T3, reverse T3 (rT3) and TSH (Throid Stimulating Hormone). When the total of T3, T4 and rT3 is low, TSH causes the release of additional T4. T4 has very little activity and is used to make T3 and rT3. RT3 has no activity. T3 is the active form. RT3 occupies binding sites of T3, and may feed back to decrease TSH. With all T3 protocols, the patient takes T3 pills so that TSH levels drop to near zero. Therefore, T4 ceases to be produced. And therefore, rT3 ceases to be produced.

Blood tests for Thyroid hormone are not reliable. A person with “normal” blood levels of thyroid hormones may have a deficiency within the cells. Deficiency is identified by low body temperature, intolerance for cold, dry skin, and other low-thyroid symptoms.

B. Dr. Denis Wilson (http://www.wilsonstemperaturesyndrome.com/Medical.htm)

Wilson's therapy is Temporary (a few months), and uses time-released T3 from any compounding pharmacy.

Theory (http://wilsonstemperaturesyndrome.com/eManual/Chapters/05WhyNotT4.cfm#Pg50): On the cellular level (not detectable in blood tests), high-levels of RT3 use up the 5’ deiodinase enzyme that otherwise would convert T4 to T3, which thus maintains low T3 in favor of T4 and RT3. RT3 must be eliminated to break the cycle.

On Wilson's protocol, you begin with a 7.5 mcg dose every 12 hours and increase dosage incrementaly every few days until low-thyroid symptoms go away, then you stay at that highest dose for 3 weeks, then you incrementaly reduce the dosage. If low-thyroid symptoms return after you reduce the dosage to zero, you do another cycle. The amound of T3 required (to make low-thyroid symptoms go away) should be less and less with each cycle.

C. Australian pharmacy (http://www.custommedicine.com.au/blog/2007/04/17/reverse-t3-dominance/)

This is a Temporary therapy, similar to Wilson’s protocol since it uses time-released T3, exept it uses a steady, low dosage with no cycling. Start with 10 mcg per day. Monitor energy levels and body temperature, and increase dosage accordingly. Do not exceed 15 mcg per day. Over 2 to 3 months of therapy, symptoms should improve and rT3 levels shouold decrease.

D. John Lowe (http://www.thyroidscience.us/info/12%20Chapter%207.Thyroid.pdf)

This is a Permanent therapy, taken for the rest of your life, as far as I can determine.

Dr. Lowe uses regular Cytomel T3, not time-release. The full dose is taken all at once, one time per day. T3 blood levels spike after dosage and fall later, but the tissue levels remain elevated. Heart symptoms may occur after dosage but are safe and temporary.

The starting dose of T3 is generally equal to the amount of thyroid hormone that the thyroid itself would produce per day. The patient increases the dosage in small increments (at intervals of a few days or a week or two) until reaching the “therapeutic window” where there are no symptoms of high thyroid or low thyroid.

E. Protocol based on the Yahoo user group. (http://thyroid-rt3.com/)

Similar to the Dr. Lowes protocol this is a Permanent therapy with Cytomel T3 (not time-released). Daily dosage is taken in divided doses, 4 times per day. After about 12 weeks of treatment, rT3 clears from the T3 receptors. Results can appear suddenly at that point, and dosage may need to be cut in half (and may need to be reduced almost completely for a day or 2).

F. D1 management in lieu of T3 therapy.

Human iodothyronin deiodinases D1 and D2 are enzymes that reduce T3, increase T4, increase rT3 and increase TSH. It has been stated in this forum that you can “work on D1 enzyme and RT3 will take care of itself (http://musclechatroom.com/forum/showthread.php?t=2666&highlight=wilson+t3+reset).”

==========

Are these descriptions accurate? What are the options for D1 therapy instead of T3 therapy? And will the Wilson's protocol work with once-daily Cytomel instead of time-released T3?



.

[JanSz]

Hopefully I understand dr Mariano's concerns about T4.
He wants to have T4 at about mid range.

dr Mariano worries about ample T4 level,
because of blood-brain barrier.

Possibly he should not worry about T4 levels (that much).
================================================== =====


http://www.thyroidscience.com/letters/letters.htm#Subject:_What_is_prealbumin

Letter to the Editor

Subject: What is prealbumin
Date: November 24, 2009
From: Author prefers anonymity
To: editor@thyroidscience.com

My doctor gave me my lab results yesterday. I know what most of the thyroid tests are, but I’ve never heard of one. It is the “prealbumin.” Do you know what this is? My level was 0.20 g/L, and the range is listed as 0.18-to-0.39 g/L. Do you know what this result means?

Reply by Dr. John C. Lowe, Editor-in-Chief of Thyroid Science (November 24, 2009)

Dear Bob: We have a newer name for prealbumin, which is “transthyretin.” Transthyretin is a protein that is important to thyroid hormone regulation of the brain. The protein transports thyroid hormone across the blood-brain barrier; that is, from the blood outside the brain to the blood inside brain. Transthyretin that transports thyroid hormone in the blood is produced in the liver, but transthyretin that transports thyroid hormone across the blood brain barrier is produced in a structure called the “choroid plexus” at the base of the brain.

When I say that the protein transports thyroid hormone across the blood-brain barrier, I mean that it transports both T4 and T3. This is important to understand. The reason is that many clinicians mistakenly think that transthyretin transports only T4 into the brain. Based on this mistaken belief, these clinicians also mistakenly believe that normal brain function depends on patients including T4 in their thyroid hormone therapy. This, however, is patently false. (Elsewhere, I extensively documented that transthyretin transports both T4 and T3 into the brain. I published one article in 2005 and the second in 2006.)

You wrote that your transthyretin level was 0.20 g/L (20 mg/dL). With a range of 0.18-to-0.39 g/L (18-to-39 mg/dL), your level is very low; it’s in the lower 4th of the range.

Some diagnosticians would say this level means you’re not producing an optimal amount of transthyretin; others would say that you’re producing plenty. I don’t think we have enough studies to tell us which of those diagnosticians are right and wrong.

What we can tell from your level is that you’re producing the protein and your most likely getting thyroid hormone into your brain. We don’t have tests commercially available that measure the amount of thyroid hormone that is bound to one’s transthyretin. That piece of information would be valuable. The reason is that dioxins and PCBs can displace thyroid hormone from the protein. As a result, these chemical contaminants can ride into the brain on the protein. The more of the contaminants that ride the protein into the brain, the less T4 and T3 are likely to reach brain cells. Once inside the brain, dioxins and PCBs bind to T3 receptors on genes. The binding alters the pattern of codes that the genes send out to the work part of the cell for the production of proteins. I believe this phenomenon is responsible for some of the cognitive and mood problems of people contaminated with dioxins and PCBs, which toxicologists have told me is each of us. (I heavily documented the thyroid-disrupting effects of these pollutants in the “Environmental Contaminants” section in Chapter 2.4, “Thyroid Hormone Deficiency,” of The Metabolic Treatment of Fibromyalgia [available in the publisher's E-Chapter section].)

I assume that you wrote to me about your transthyretin level from concern about your thyroid hormone status. However, some clinicians order the test to learn whether a patient is ingesting enough protein. Transthyretin is a “glycoprotein,” which means it is a carbohydrate combined with a protein. Of all the proteins in the blood, it’s transthyretin that is most useful in telling whether a person has a protein deficiency. The half life of the protein is about two days, so it’s level in the blood changes quickly when someone markedly decreases or increases protein intake, digestion, and/or absorption.

You didn’t say whether you ate little to no protein for several days before your blood was drawn to measure your transthyretin. If you ate little to none, that might account for your low-range transthyretin level. If that is the case, you should talk with your clinician about measuring your transthyretin level again after you eat 50-to-75 grams of protein each day for several days. Your tranthyretin level might then be higher. But keep in mind that inflammation and infection can also lower transthyretin level, and severe kidney disease and the use of glucocorticoid (such as prednisone or prednisolone) can raise your level. I hope this is helpful to you.

[EIC]

Excellent post, Jan, on a number of fronts.

[JanSz]

Presumptions of the Endocrinology Specialty: Instability of Desiccated Thyroid, Dangers of T3, and the Safety and Effectiveness of T4-replacement

Presumptions of the Endocrinology Specialty: Instability of Desiccated Thyroid, Dangers of T3, and the Safety and Effectiveness of T4-replacement

Dangers of T3

The endocrinology specialty has long opposed the use of products that contain T3. The basis of its opposition, so it claims, is the resulting brief peak blood level of T3. Members of the specialty glibly state that the peak level is in the "thyrotoxic range"[84,p.1225] and that this peak level causes heart palpitations that trouble patients. They further state that the peak level may adversely affect the heart. But, these members resound, by using Synthroid patients can avoid these problems.

The specialty’s claim that T3 causes these problems is a mere presumption; it is contradicted by the reports of researchers with extensive clinical experience with T3. Psychiatric researchers whose patients use T3 point out that it is generally well-tolerated.[35] The experience of my research group agrees with this observation. For some fifteen years, our treatment team has worked directly with hundreds of patients using combined T4/T3 products or T3 alone. Our observations during that time dispute the warning that palpitations are a problem for patients who use T3-containing products. Palpitations in these patients are exceedingly rare. When a patient has experienced palpitations, they have been minor and of little or no concern to the patient. The palpitations have also been of no clinical significance. It’s noteworthy that the researchers of the four studies, as well as those of three other studies comparing the effectiveness of T4 and T4/T3-replacement, didn’t report that their study patients were troubled by palpitations.[1][2][3][4][5][6][7]

I can find no study that members of the specialty have conducted confirming its prediction of adverse effects from T3. Only last year, endocrinologists Kaplan, Sarne, and Schneider wrote: ". . . the possible long-term risks of elevated or fluctuating T3 levels have not been evaluated."[19,p.4541]

Systematic studies have not conclusively ruled out long-term adverse effects. But many patients have used T3 for many years without apparent adverse effects. We have, then, a positive anecdotal record and no long-term safety studies showing that T3 is harmful. Regardless, the specialty has warned of potential harm in a manner that has generated irrational fear of T3 among physicians. It’s common, for example, for patients who’ve asked their doctors to prescribe T3 to hear the reply, "If you take T3, you’re going to have a heart attack and die!"[48,p.10]

It goes without saying, of course, that caution is necessary with patients who have fragile cardiac conditions. This is especially true when such a patient is using a product containing T3, since T3 directly affects the myocardium.[66] But potential harm from T3 is not actual harm, and the endocrinology specialty has so blurred the distinction that most other physicians—and perhaps they themselves—don’t know the difference.

[bgnb]

Presumptions of the Endocrinology Specialty: Instability of Desiccated Thyroid, Dangers of T3, and the Safety and Effectiveness of T4-replacement

Presumptions of the Endocrinology Specialty: Instability of Desiccated Thyroid, Dangers of T3, and the Safety and Effectiveness of T4-replacement

Dangers of T3


It goes without saying, of course, that caution is necessary with patients who have fragile cardiac conditions. This is especially true when such a patient is using a product containing T3, since T3 directly affects the myocardium.[66] But potential harm from T3 is not actual harm, and the endocrinology specialty has so blurred the distinction that most other physicians—and perhaps they themselves—don’t know the difference.

more of a concern in the elderly as well, when the kidneys are no longer
as effective at removing T3 ...

D.A. Question for this whole thread:

If T4 --> rT3 and T4 reserves last up to 100 days, then wouldn't
going on T3 only for 100 days use up the T4 reserves and clear
out remaining rT3 and then you could slowly reintroduce the T4
and wean off the T3 ... assuming of course, that at that point you
still needed any thyroid supplementation?

[JackBauer]

more of a concern in the elderly as well, when the kidneys are no longer
as effective at removing T3 ...

D.A. Question for this whole thread:

If T4 --> rT3 and T4 reserves last up to 100 days, then wouldn't
going on T3 only for 100 days use up the T4 reserves and clear


Isn't 100 days something like 13 half lives? I think you really only need like 5-6 to clear your system out almost completely.

[bgnb]

Isn't 100 days something like 13 half lives? I think you really only need like 5-6 to clear your system out almost completely.

I believe that refers to the half life of exogenous T4 not what's
stored in the thyroid.

[JackBauer]

I believe that refers to the half life of exogenous T4 not what's
stored in the thyroid.

But if you supplement with T3, your TSH comes down, and T4 stops being produced.

(I think, right?)

[EIC]

But if you supplement with T3, your TSH comes down, and T4 stops being produced.

(I think, right?)

If you take enough, yes. Though, more accurately, T4 production would probably drop really, really low. I doubt it would stop completely.

[bgnb]

But if you supplement with T3, your TSH comes down, and T4 stops being produced.

(I think, right?)

that's what I assuming ... but my understanding is that there is
still lots of T4 stored ... so it may take time to get that cleared
out so both T3 and rT3 are being produced and only (or mainly)
the exogenous T3 we take would be used exclusively ...

that's what I was wondering -- whether that would work and how
long it would take to work ...

:)

[00slotiv]

that's what I assuming ... but my understanding is that there is
still lots of T4 stored ... so it may take time to get that cleared
out so both T3 and rT3 are being produced and only (or mainly)
the exogenous T3 we take would be used exclusively ...

that's what I was wondering -- whether that would work and how
long it would take to work ...

:)

Appears top be the case. After about three months it looks like my T4 is about the same while T3 is way up and reverse T3 is down but still maybe too high. Will have more results soon.

Bob

[bgnb]

Appears top be the case. After about three months it looks like my T4 is about the same while T3 is way up and reverse T3 is down but still maybe too high. Will have more results soon.

Bob

interesting to see your results ... I have been on T3 for 50+ days and
starting to notice more improvement but my Testosterone is still low
so that's still dragging me down ...

[flyfish1000]

Dr Mariano a respected psychiatrist argues that high RT3 is not a problem if the Free T3 is in the normal range. He treats thyroid with T4 only. Can it be argued that a high RT3 with a normal free T3 level is still a concern.

[hebsie]

...an interesting factoid, here in Canada, well Ontario anyways, we cannot get a RT3 test. We can't even pay for it if we want it, the labs have it as a discontinued test.

If it's really all that important, why wouldn't our doctors want to test for it too?? Just thinking out loud here...hebs

[LowT]

I respect Dr. Mariano greatly and I'm not a doc...I can only relate my own experience.

My FT4 was ABOVE RANGE...as in, actually out of lab range. My FT3 was mid range and my RT3 was over 500 (top of range 350).

My body temps were in the 96's, resting heart rate into the 40s at times and severe constipation and fatigue. Cytomel was the only thing that fixed me.

RT3 is certainly a real issue for those suffering from it.

Additionally, I've read that some lab assays cannot differentiate RT3 from FT3 on the T3 portion of the test. I don't know if this is true but if so, it would mean without an RT3 test there would be no way to know what is truely happening.

[LeanGuy]

My FT4 was ABOVE RANGE...as in, actually out of lab range. My FT3 was mid range and my RT3 was over 500 (top of range 350).

You obviously have a problem converting T4->T3 and need cytomel for this reason, but how do you know your problem is RT3 and not FT3? Maybe you need upper range FT3 instead of mid-range?

[EIC]

I have tremendous respect for Dr. M. However, I always thought that if he wanted to demonstrate to a concerned patient that rT3 is really nothing to worry about, he should include the lab in his orders and show the patient that it either does not elevate, or if elevated, does not prevent the patient from feeling well.

[garcia]

I have great respect for Dr Mariano, but I have to disagree on this one.
If you look at my labs below you can see that my (free) T3 is completely normal. But my RT3 is out of range. Subjectively I feel very hypothyroid.

So how how to treat? Well adding more T4 won't work since my T4 is already out of range.


http://i64.photobucket.com/albums/h168/jgarcia3788/Thyroid.jpg

[flyfish1000]

You feel bad with high RT3 but you don't balance that with how you have felt with a low RT3 before or after. Without before and after low and high readings It could be argued that there could be other reasons for the way you feel. What evidence is there that high RT3 can make you feel bad?

[EIC]

We need to be clear here on one thing: Dr. M agrees that rT3 exists. He also agrees that if high, rT3 will interrupt healthy thyroid function. The only sticking point is that he does not believe rT3 will be chronically elevated; he believes it is only a transient state that will diminish naturally shortly thereafter.

I have long suspected that this concept is based on studies done of people who experienced a single bout of very intense stress (i.e., death in the family, divorce, surgery). In such cases, I don't doubt that rT3 will diminish on its own several weeks later relative to where it was before the stressful episode. But what about people who are under chronic stress? It makes no sense to me that their rT3 would just magically reset itself at an arbitrary date a few weeks after the stressful event started.

[garcia]

We need to be clear here on one thing: Dr. M agrees that rT3 exists. He also agrees that if high, rT3 will interrupt healthy thyroid function. The only sticking point is that he does not believe rT3 will be chronically elevated; he believes it is only a transient state that will diminish naturally shortly thereafter.

I have long suspected that this concept is based on studies done of people who experienced a single bout of very intense stress (i.e., death in the family, divorce, surgery). In such cases, I don't doubt that rT3 will diminish on its own several weeks later relative to where it was before the stressful episode. But what about people who are under chronic stress? It makes no sense to me that their rT3 would just magically reset itself at an arbitrary date a few weeks after the stressful event started.

Great post EIC! Thanks for clearing that up. Well all I can say is my "stress" happened 4 years ago (chronic infection), but the stress is ongoing so the RT3 stays elevated.

It isn't going to fix itself until I get rid of the stressor.

[hardasnails1973]

BY treating with low dosages of t-3 clearing reverse t3 we have had numerous people on antidepressants who have been on 2-3 different kinds. Now they are off after average of 10 year usage..That says it right there,

[JanSz]

BY treating with low dosages of t-3 clearing reverse t3 we have had numerous people on antidepressants who have been on 2-3 different kinds. Now they are off after average of 10 year usage..That says it right there,

As long as doctor recognizes that high rT3 is undesirable and treatable condition,
his patient have a fighting chance.


...

[TESTOCULES]

You feel bad with high RT3 but you don't balance that with how you have felt with a low RT3 before or after. Without before and after low and high readings It could be argued that there could be other reasons for the way you feel. What evidence is there that high RT3 can make you feel bad?

The evidence is that once you clear it by being on a t3 only regimin for about 3 months, all your unexplained hypo symptoms disappear.

[pmgamer18]

Most people with a lab saying there RT3 is high feel fine I am one of them. And if your ratio if FT3 to RT3 is bad and you feel bad. Even if you do T3 only meds to get the RT3 down when you stop this and go back to your old meds it will go back up. You need to fix why your RT3 is high and for most this is stress in your life. For me it is due to the stress of sugary. Read this Cut and Paste about RT3 from STTM site.
=====================================
A healthy thyroid produces the following hormones: T4, T3, T2, T1 and calcitonin. T4, a storage hormone and the most abundant, is meant to convert to T3, the most active hormone. T3 is also produced directly.

In any situation where your body needs to conserve energy, such as emotional, physical, or biological stress, your thyroid will properly convert any excess T4 to the inactive Reverse T3 (RT3) as a way to clear out the extra T4.

When stress is excessive, your adrenal glands produce high amounts of cortisol to help you cope. The excess cortisol inhibits the conversion of T4 to T3, and instead produces even larger amounts of RT3.

Because an over-abundance of RT3 (RT3 dominance) blocks the ability of the cell receptors to receive T3, hypothyroid symptoms are the result, including a lowered body temperature, fatigue, anxiety, weight gain and a host of other symptoms.

With labwork, you are not necessarily looking for a RT3 result high in the range. Instead, you are looking for a problem in the ratio between the RT3 and the Free T3.
To read about RT3 problems, you can read patient Nick Foote’s compilation of Questions and Answers gleaned from the RT3 Yahoo group.

http://thyroid-rt3.com/

[JanSz]

Most people with a lab saying there RT3 is high feel fine I am one of them. And if your ratio if FT3 to RT3 is bad and you feel bad. Even if you do T3 only meds to get the RT3 down when you stop this and go back to your old meds it will go back up. You need to fix why your RT3 is high and for most this is stress in your life. For me it is due to the stress of sugary. Read this Cut and Paste about RT3 from STTM site.
=====================================
A healthy thyroid produces the following hormones: T4, T3, T2, T1 and calcitonin. T4, a storage hormone and the most abundant, is meant to convert to T3, the most active hormone. T3 is also produced directly.

In any situation where your body needs to conserve energy, such as emotional, physical, or biological stress, your thyroid will properly convert any excess T4 to the inactive Reverse T3 (RT3) as a way to clear out the extra T4.

When stress is excessive, your adrenal glands produce high amounts of cortisol to help you cope. The excess cortisol inhibits the conversion of T4 to T3, and instead produces even larger amounts of RT3.

Because an over-abundance of RT3 (RT3 dominance) blocks the ability of the cell receptors to receive T3, hypothyroid symptoms are the result, including a lowered body temperature, fatigue, anxiety, weight gain and a host of other symptoms.

With labwork, you are not necessarily looking for a RT3 result high in the range. Instead, you are looking for a problem in the ratio between the RT3 and the Free T3.
To read about RT3 problems, you can read patient Nick Foote’s compilation of Questions and Answers gleaned from the RT3 Yahoo group.

http://thyroid-rt3.com/

From the link you posted:

http://thyroid-rt3.com/


Question:
Do I need T4 at all?, otherwise known as Can I stay on T3 permanently???


Answer:
In a nutshell NO.

//////////////////

[charliebizz]

BY treating with low dosages of t-3 clearing reverse t3 we have had numerous people on antidepressants who have been on 2-3 different kinds. Now they are off after average of 10 year usage..That says it right there,

ok but what keeps the rt3 from going back up after stopping the t3

[charliebizz]

From the link you posted:

http://thyroid-rt3.com/


Question:
Do I need T4 at all?, otherwise known as Can I stay on T3 permanently???


Answer:
In a nutshell NO.

//////////////////so how long is one supposed to stay on t3 for.my t3 and t4 look good now in my labs but my rt3 is up out of range.so in my case what would i do once my rt3 cleared would i need to co on a t3/t4 combo.or would i just ween off the t3 if i got rid of the stress that was causing my rt3

[TryingToFix]

Most people with a lab saying there RT3 is high feel fine I am one of them. And if your ratio if FT3 to RT3 is bad and you feel bad. Even if you do T3 only meds to get the RT3 down when you stop this and go back to your old meds it will go back up. You need to fix why your RT3 is high and for most this is stress in your life. For me it is due to the stress of sugary. Read this Cut and Paste about RT3 from STTM site.
=====================================
A healthy thyroid produces the following hormones: T4, T3, T2, T1 and calcitonin. T4, a storage hormone and the most abundant, is meant to convert to T3, the most active hormone. T3 is also produced directly.

In any situation where your body needs to conserve energy, such as emotional, physical, or biological stress, your thyroid will properly convert any excess T4 to the inactive Reverse T3 (RT3) as a way to clear out the extra T4.

When stress is excessive, your adrenal glands produce high amounts of cortisol to help you cope. The excess cortisol inhibits the conversion of T4 to T3, and instead produces even larger amounts of RT3.

Because an over-abundance of RT3 (RT3 dominance) blocks the ability of the cell receptors to receive T3, hypothyroid symptoms are the result, including a lowered body temperature, fatigue, anxiety, weight gain and a host of other symptoms.

With labwork, you are not necessarily looking for a RT3 result high in the range. Instead, you are looking for a problem in the ratio between the RT3 and the Free T3.
To read about RT3 problems, you can read patient Nick Foote’s compilation of Questions and Answers gleaned from the RT3 Yahoo group.

http://thyroid-rt3.com/

Thanks, pmgamer18 for the info and thread. Great read.

[JanSz]

ok but what keeps the rt3 from going back up after stopping the t3

I think it may be analogous to TRT we need it forewer.

Reason that we have to much rT3 is because our deidinases are not working as they should (no matter how cleverly we are supporting it).

I am afraid that stopping thyroid hormones supplementation (gradually please), will return one to original state (or possibly worse).

==============================================
OTOH,
we have a known list of items that are conducive to increased rT3.

Surgery is probably the most important one.

So after the stressful events are over, it may be a worth trying to wean of off thyroid hormones,
at least partially.

I admit that living with out fall-back store of T4 is on edge, and may be a source of stress on its own, for certain individuals.

..

[TryingToFix]

Most people with a lab saying there RT3 is high feel fine I am one of them. And if your ratio if FT3 to RT3 is bad and you feel bad. Even if you do T3 only meds to get the RT3 down when you stop this and go back to your old meds it will go back up. You need to fix why your RT3 is high and for most this is stress in your life. For me it is due to the stress of sugary. Read this Cut and Paste about RT3 from STTM site.
=====================================
A healthy thyroid produces the following hormones: T4, T3, T2, T1 and calcitonin. T4, a storage hormone and the most abundant, is meant to convert to T3, the most active hormone. T3 is also produced directly.

In any situation where your body needs to conserve energy, such as emotional, physical, or biological stress, your thyroid will properly convert any excess T4 to the inactive Reverse T3 (RT3) as a way to clear out the extra T4.

When stress is excessive, your adrenal glands produce high amounts of cortisol to help you cope. The excess cortisol inhibits the conversion of T4 to T3, and instead produces even larger amounts of RT3.

Because an over-abundance of RT3 (RT3 dominance) blocks the ability of the cell receptors to receive T3, hypothyroid symptoms are the result, including a lowered body temperature, fatigue, anxiety, weight gain and a host of other symptoms.

With labwork, you are not necessarily looking for a RT3 result high in the range. Instead, you are looking for a problem in the ratio between the RT3 and the Free T3.
To read about RT3 problems, you can read patient Nick Foote’s compilation of Questions and Answers gleaned from the RT3 Yahoo group.

http://thyroid-rt3.com/

So with my labs at the following levels:
TSH 2.08 mIU/L
FT4 1.40 ng/dL
RT3 27 ng/dL
FT3 354 pg/dL

So ratio FT3/RT3 (354/27) = 13 which is less than the 20 recommend on the link. Thus if I understood all material; based on labs and symptoms I have what is described, thyroid is not getting to the receptors.

Looks like I need the RT3 around 18 to be at the 20 multiple.

[EIC]

So with my labs at the following levels:
TSH 2.08 mIU/L
FT4 1.40 ng/dL
RT3 27 ng/dL
FT3 354 pg/dL

So ratio FT3/RT3 (354/27) = 13 which is less than the 20 recommend on the link. Thus if I understood all material; based on labs and symptoms I have what is described, thyroid is not getting to the receptors.

Looks like I need the RT3 around 18 to be at the 20 multiple.

Is that really how it's done? Just divide the raw numbers of FT3 by rT3 to get the ratio? If so, mine is unbelievably piss poor: FT3 = 275 and rT3 = 27 for a FT3:rT3 ratio of ~10. Holy cow that is terrible.

[TryingToFix]

Is that really how it's done? Just divide the raw numbers of FT3 by rT3 to get the ratio? If so, mine is unbelievably piss poor: FT3 = 275 and rT3 = 27 for a FT3:rT3 ratio of ~10. Holy cow that is terrible.

That was my understanding off the thyroid link that pmgamer18 provided, under 'How is it diagnosed' section.

Maybe pmgamer18 will get a chance to confirm the calculations and understanding of it.

[JanSz]

Best available to me, research done on old men without any thyroid hormones supplementation.

http://jcem.endojournals.org/cgi/reprint/90/12/6403.pdf

That research is not friendly to produce ratios.
Instead individual hormones are presented.

There is two figures sumarizing results, fig #1 & fig #2.
Those figures are also attached on my post #47
http://musclechatroom.com/forum/showpost.php?p=35410&postcount=47
===========================================

Limits of normal (natural no supplementation) old healthy adults
From Fig #1
T3>1.35 nmol/L=87.7 ng/dL
rT3< 0.32 nmol/L=20.8 ng/dL

Fig #2 gives ranges for normal (natural no supplementation) healthy adults
RT3(0.12-0.32)nmol/L=(7.8-20.8)ng/dL
FT4(11-25)pmol/L=(0.85-1.94)ng/dL (these guys are actually making use of their naturally produced T4, they must have raw material to make T3)
=============================================

Using those figures and numbers we may derive
desirable levels for people who are supplementing thyroid hormones.

For starters, FT4 requirements is gone.

For starters,
T3>1.35 nmol/L=87.7 ng/dL
rT3< 0.32 nmol/L=20.8 ng/dL

is a absolutely minimum requirement.

Then
look at fig#1 and make judgement.

I aim at low range on rT3
RT3(0.12-0.32)nmol/L=(7.8-20.8)ng/dL

getting to TT3
I have to remind my self that the research was done on old, very old men.

2.2 nmol/L=2/0.0154=143 ng/dL

So if I am very old men, and if I do not supplement with thyroid hormones,
my chances are best when I have
TT3=143 ng/dL

And some of those guys actually had that much, so they lived the longest.

For younger, thyroid hormones supplementing folks, lef.org advises upper third of range.

In my tests TT3(60-181)ng/dL

middle of that upper 1/3 range is

60+(181-60)/6*5=161ng/dL

One must remember that other labs may have different ranges, so the value applicable to their test report may have to be recalculated.
==================================

Recap
when supplementing, do not support enemy
do not supply T4, you already have too much of it and only able to make rT3 from it.

minimum to live with some chance for old age (both required at the same time):
TT3>1.35 nmol/L=87.7 ng/dL
rT3< 0.32 nmol/L=20.8 ng/dL

desirable:
RT3(0.12-0.32)nmol/L=(7.8-20.8)ng/dL
TT3=~160 ng/dL

note that in all this discussions, nobody worried about FreeT3

and (specially) FreeT4.


.................

[Dr. John Crisler]

Dr Mariano a respected psychiatrist argues that high RT3 is not a problem if the Free T3 is in the normal range. He treats thyroid with T4 only. Can it be argued that a high RT3 with a normal free T3 level is still a concern.

There is no doubt many simply do not convert T4 to T3 adequately. Even with fT3 well up in range, high rT3 can block its effects.

But since he only gives T4, then if T3 is in range, the patient is indeed converting well.

Adding T3 not only increases same, and mass action overcomes rT3, it also increases the activity of enzyme D1. This improves health by stimulating T4 to T3 conversion.

[Dr. John Crisler]

I respect Dr. Mariano greatly and I'm not a doc...I can only relate my own experience.

My FT4 was ABOVE RANGE...as in, actually out of lab range. My FT3 was mid range and my RT3 was over 500 (top of range 350).

My body temps were in the 96's, resting heart rate into the 40s at times and severe constipation and fatigue. Cytomel was the only thing that fixed me.

RT3 is certainly a real issue for those suffering from it.

Additionally, I've read that some lab assays cannot differentiate RT3 from FT3 on the T3 portion of the test. I don't know if this is true but if so, it would mean without an RT3 test there would be no way to know what is truely happening.If you can get a rT3, then you know its influence. Since true experts treat thyroid to effect, it's okay to elevate T3 to a point the patient is adequately treated. So even IF the proportionately smaller amount of rT3 were included, it doesn't matter.

[Dr. John Crisler]

We need to be clear here on one thing: Dr. M agrees that rT3 exists. He also agrees that if high, rT3 will interrupt healthy thyroid function. The only sticking point is that he does not believe rT3 will be chronically elevated; he believes it is only a transient state that will diminish naturally shortly thereafter.

I have long suspected that this concept is based on studies done of people who experienced a single bout of very intense stress (i.e., death in the family, divorce, surgery). In such cases, I don't doubt that rT3 will diminish on its own several weeks later relative to where it was before the stressful episode. But what about people who are under chronic stress? It makes no sense to me that their rT3 would just magically reset itself at an arbitrary date a few weeks after the stressful event started.That is ascertained through proper taking of Medical History.

[chilln]

ok but what keeps the rt3 from going back up after stopping the t3

Different things for different people.

For some, their RT3 drops only after boosting their cortisol (supps or sleep), because their T3 is only converting into RT3 because there isn't enough cortisol to transport thyroid hormone T3 into cells, thus causing excess T3 to convert into RT3.

For others, their RT3 only stays lowered because they're on T3 supps for life, because their D1 enzymes are downregulated by genetic aging, no matter they try.

For others, their RT3 drops when their stressors are removed and their high cortisol becomes available for use in transporting thyroid hormone.

Etc...

[charliebizz]

Different things for different people.

For some, their RT3 drops only after boosting their cortisol (supps or sleep), because their T3 is only converting into RT3 because there isn't enough cortisol to transport thyroid hormone T3 into cells, thus causing excess T3 to convert into RT3.

For others, their RT3 only stays lowered because they're on T3 supps for life, because their D1 enzymes are downregulated by genetic aging, no matter they try.

For others, their RT3 drops when their stressors are removed and their high cortisol becomes available for use in transporting thyroid hormone.

Etc...

ok well say one with good thyroid labs with the exception of high rt3 starts treatment with t3 and also figure out the stressor causing the rt3 issue once the rt3 is cleared how does one go about weening off the t3

[wondering]

This is NOT a true statement...

Dr. M bases treatment on each individual. He does NOT however just prescribe Armour automatically. His positon is that due to the immediate availability of T3 in Armour or straight T3... it CAN be a burden on stressed adrenals and not just reveal an issue with them, but actually contribute to stress placed on them. So, he will prescribe T4 only in some cases and if conversion to T3 is ok and patient feels fine leave it at that.

But he will use T3 or natural Thyroid if he thinks patient will be better served.



Dr Mariano a respected psychiatrist argues that high RT3 is not a problem if the Free T3 is in the normal range. He treats thyroid with T4 only. Can it be argued that a high RT3 with a normal free T3 level is still a concern.

[EIC]

That is ascertained through proper taking of Medical History.

I may have misspoke. When asked about rT3, Dr. M referred me to studies which showed that elevated rT3 only occurs in a transient state and reduces to healthy levels after a couple of weeks. I suspect that such studies are probably based on analyses of people who underwent a brief, but intense, period of physical or emotional stress.

I find it hard to believe that studies have been conducted on people with chronic stress or health problems showing that elevated rT3 is only a transient problem.

[EIC]

There is no doubt many simply do not convert T4 to T3 adequately. Even with fT3 well up in range, high rT3 can block its effects.

But since he only gives T4, then if T3 is in range, the patient is indeed converting well.

Adding T3 not only increases same, and mass action overcomes rT3, it also increases the activity of enzyme D1. This improves health by stimulating T4 to T3 conversion.

I think this is an excellent point and nicely explains why people who take combo T3/T4 meds tend to do much better than those on T4 alone; better even that what could be explained by the mere addition of straight T3. In other words, T3/T4 seems to outpace T4 in improving patient's health not only by the addition of straight T3 but because of the additional conversion of that T4 that the T3 itself allows. We have observed the effect; now we know the mechanism.

[Dr. John Crisler]

I may have misspoke. When asked about rT3, Dr. M referred me to studies which showed that elevated rT3 only occurs in a transient state and reduces to healthy levels after a couple of weeks. I suspect that such studies are probably based on analyses of people who underwent a brief, but intense, period of physical or emotional stress.

I find it hard to believe that studies have been conducted on people with chronic stress or health problems showing that elevated rT3 is only a transient problem.If it is a transient state, that is a different matter. But these are people who come in feeling horribly for an extended period of time. When we assess their thyroid function, rT3 is elevated. It is a smoking gun.

Nutritional deficiencies leading to upregulation of enzyme D3 and downregulation of enzyme D1 are not transient.

Supplementing T3 for a time encouraging the reverse of the above (as nutritional deficiencies are being addressed). And the patient is then able to make it through his/her day--in this economy.

Doctors are not able to remove stress from a patient's life in one office visit. LOL

Yes, the studies mentioned are comparing apples and oranges.

[JanSz]

http://www.journals.elsevierhealth.com/periodicals/bon/article/S8756-3282(08)00169-5/abstract

Most circulating active thyroid hormone (T3) is derived from outer ring deiodination of thyroxine (T4) mediated by the type 1 deiodinase enzyme (D1).

The D2 isozyme regulates intra-cellular T3 supply and determines saturation of the nuclear T3-receptor (TR),

whereas a third enzyme (D3) inactivates T4 and T3 to prevent hormone availability and reduce TR-saturation.

================================================== =========

http://endo.endojournals.org/cgi/content/abstract/147/7/3580

Essentially all serious illness is associated with a decrease in circulating T3, a condition known as the nonthyroidal illness syndrome.

Substantial evidence suggests that a contributing factor to this syndrome is a cytokine-induced decrease in hepatic type 1 iodothyronine deiodinase (D1), an enzyme that converts T4 to T3. The type 1 deiodinase is induced at the transcriptional level by T3, but illness-associated cytokines block this induction, resulting in decreased T3 and hence a further decline in D1 expression. We demonstrated that IL-1 blocks the ability of T3 to induce D1 in rat hepatocyte primary cultures and that forced expression of steroid receptor co- activator 1 (SRC-1) prevents this cytokine effect. This led us to test whether forced hepatic expression of SRC-1 can prevent the nonthyroidal illness syndrome in vivo.

=============================================

Ok, so, we do not want IL-1

=============================================
http://joe.endocrinology-journals.org/cgi/content/abstract/167/3/505

Effects of proinflammatory cytokines on anterior pituitary 5'-deiodinase type I and type II

A Baur, K Bauer, H Jarry, and J Kohrle

Cytokines are locally produced in the anterior pituitary and act through para-/autocrine mechanisms to modulate cell growth and hormone production. 5'-Deiodinases type I (D1) and type II (D2) are also expressed in the anterior pituitary and play an integrative role in the regulation of hormone production and pituitary feedback. D1 activity is known to be regulated by proinflammatory cytokines in liver and thyroid. Therefore, we examined the effects of IL-1 beta, IL-6 and TNF alpha on 5'-deiodinase activities in reaggregates of rat anterior pituitaries and rat somatomammotroph GH3 cells cultured alone, or in a bicameral culture system together with the murine folliculo-stellate (FS) cell line TtT/Gf. In reaggregate cultures of rat anterior pituitaries IL-1 beta stimulated D1 and D2 dose-dependently and D2 activity was increased by TNF alpha. When GH3 cells were cocultured with TtT/Gf cells, D2 activities were 2.3-fold lower than in GH3 cells cultured alone. TNF alpha (50 ng/ml) and IL-6 (100 U/ml) stimulated D2 in GH3 cells when the cells were cultured alone and treated with these cytokines for 24 h. When TtT/Gf cells in the coculture model were treated with IL-1 beta, TNF alpha and IL-6, no effect on D1 or D2 activities in GH3 cells was observed. In male, adult rats a single LPS injection (i.p.) stimulated D2 and D1 activities in the anterior pituitary, and decreased liver D1 activities and serum TSH levels. In vitro, LPS stimulation of the coculture model of GH3 and FS cells also increased D1 activity. Electrophoretic mobility shift assays (EMSAs) revealed that IL-1 beta and TNF alpha activate the transcription factor NF kappa B in reaggregates of rat anterior pituitaries and in TtT/Gf cells cultured alone or cocultured with GH3 cells. Taken together, these findings imply that in anterior pituitary cells 5'-deiodinase activities are stimulated by locally produced cytokines in a para-/autocrine manner but cell types other than FS cells seem to mediate some of the effects.

================================================== ====

I am not clear what stimulates what, but when we are faced with low TT3 and high rT3 we have to take a closer look at cytokines.

What is LPS?
....
================================================== ====

http://www.lef.org/protocols/prtcl-146a.shtml

Pro-Inflammatory Cytokine--------- ------Optimal Anti-Inflammatory Range ---------------
----------------------------------------------Quest-------------------------------------------- LabCorp
Tumor necrosis factor alpha (TNF-a)-----------0-25 pg/mL------------------------------------- <8.1 pg/mL
Interleukin-1 beta (IL-1b)---------------------0-150 pg/mL----------------------------------- <15.0 pg/mL
Interleukin-6 (IL-6)--------------------------2-29 pg/mL------------------------------------- <12.0 pg/mL
Interleukin-8 (IL-8)--------------------------10-80 pg/mL----------------------------------- <32.0 pg/mL

he Importance of Cytokine Testing for Those Suffering From Chronic Illness
There are many chronic disease states that can now be managed by the proper utilization of the Inflammatory Cytokine Blood Panel. If you are elderly, or suffer from any serious disorder, these cytokine tests can enable your doctor to prescribe therapies that specifically target the inflammatory cytokine responsible for your poor state of health.

From a practical standpoint, if you suffer from congestive heart failure, and your levels of TNF-a remain persistently high, you may ask your doctor to prescribe the drug Enbrel®, which specifically counteracts the destructive effects of TNF-a.

If you suffer from cancer and your levels of IL-6 remain persistently high, you may consider high dose DHEA or asking your doctor to prescribe a bisphosphonate drug (such as Zometa® that protects against bone destruction that releases excess IL-6 into the body. Those with prostate, certain types of breast cancer, and other hormonally driven cancer should consider other IL-6 lowering therapies (such as high dose DHA fish oil extract) in lieu of DHEA.

Some cancer and patients display elevated levels of IL-8, which induces cancer cells to express growth factors that fuel their propagation. In hepatitis C, elevated IL-8 signals interferon drug resistance. An IL-8 suppressing therapy will soon be available to Americans (it is already used in Japan).

Those with systemic inflammatory disease often manifest high levels of IL-1b. If diet, the anti-inflammatory supplements (fish oil, borage oil, DHEA, etc.) and cytokine-suppressing drugs (pentoxifylline, 400 mg twice a day) fail to suppress this destructive cytokine, then ask your doctor to prescribe the drug Arava (leflunomide), starting at the low dose of 10 mg a day.

/

http://www.lef.org/Vitamins-Supplements/ItemLCCYT/Cytokine-Panel---IL1b-IL6-IL8-TNF-Alpha-Blood-Test.html

CYTOKINE PANEL - IL1b, IL6, IL8, TNF alpha

$495.00 each

//
.

Interleukin-1 beta (IL-1b)

This test is used to identify elevated levels of Interleukin-1 beta. IL-1b is a cytokine produced principally by mononuclear phagocytes but also by various other cells types including keratinocytes, epithelium and cells of the CNS. Elevated levels of Interleukin-1 beta have been implicated in sepsis, cachexia, rheumatoid arthritis, chronic myelogenous leukemia, asthma, psoriasis, inflammatory bowel disease, anorexia, AIDS, and graft-versus-host disease associated with bone marrow transplants. IL-1B is one of the key mediators of immunobiological responses to physical stress, a pilot study showed that higher levels were associated with anxiety/panic disorder. Higher than normal levels have also been associated with a significant increased risk of myocardial infarction independent of Cardio-CRP levels.

Interleukin-6 (IL-6)

This test is used to identify elevated levels of Interleukin-6. IL-6 is a cytokine produced by many different cells including monocytes/macrophages, fibroblasts, endothelial cells, keratinocytes, mast cells, T cells and many tumor cell lines. Elevated IL-6 serum or plasma levels may occur in different conditions including sepsis, autoimmune diseases, lymphomas, AIDS, alcoholic liver disease, tumor development, Alzheimer’s disease, and in c with infections or transplant rejection. Elevated levels of IL-6 may be associated with an increased risk of heart attack, and stroke.

Interleukin-8 (IL-8)

This test is used to identify elevated levels of Interleukin-8. IL-8 is produced by stimulated monocytes, macrophages, fibroblasts, endothelial cells, keratinocytes, melanocytes, hepatocytes, chondrocytes, and a number of tumor cell lines. In many types of cells the synthesis of IL8 is strongly stimulated by IL1 and TNF-alpha. Elevated concentrations are observed in psoriasis rheumatoid arthritis, chronic polyarthritis, tumor development and Hepatitis C.

Tumor necrosis factor alpha (TNF-a)

This test is used to identify elevated levels of Tumor necrosis factor alpha. A variety of cells are shown to produce TNF- .TNF- is a growth factor for fibroblasts and stimulates the synthesis of collagenase and prostaglandin E2. Bone resorption can be induced by TNF- because it activates osteoclasts. TNF- enhances the proliferation of T cells after stimulation with IL-2. In the absence of IL-2, TNF- induces the proliferation and differentiation of beta cells. TNF- levels may be elevated in sepsis, cachexia, AIDS, Hepatitis C, transplant rejection, various infectious and autoimmune diseases.


//

[chilln]

when we are faced with low TT3 and high rT3 we have to take a closer look at cytokines.


That's a major distraction.

when we are faced with stubborn low TT3 and stubborn high rT3 we have to take a closer look at cortisol primarily, and then testosterone and GH to trigger normal repairs, as discussed in the final round of conclusions here:

http://musclechatroom.com/forum/showpost.php?p=82716&postcount=12

.

[JanSz]

That's a major distraction.

when we are faced with stubborn low TT3 and stubborn high rT3 we have to take a closer look at cortisol primarily, and then testosterone and GH to trigger normal repairs, as discussed in the final round of conclusions here:

http://musclechatroom.com/forum/showpost.php?p=82716&postcount=12

.

I see no change to current approach.
Whatever you said in your post also apply.

But I see four new items worthy of investigation.

IL-1 looks promising.

High IL-1 can be treaded with Trental (pentoxifylline, 400 mg twice a day)

It is old and inexpensive drug.

LEF suggest it for high Fibrinogen.

http://search.lef.org/cgi-src-bin/MsmGo.exe?grab_id=0&page_id=9326&query=pentoxifylline%20fibrinogen&hiword=FIBRINOGENIC%20FIBRINOGENS%20PENTOXIFYLLIN% 20fibrinogen%20pentoxifylline%20

I was using Trental in 2008
http://musclechatroom.com/forum/showthread.php?t=959

Possibly that was a reason for my relatively reasonable rT3 level (prior to me starting campaign to get it even lower).

//

[JanSz]

In preparation for my prostate surgery I received information on Cytomel-T3 and Medrol that may be useful to keep here.

Official reprint from UpToDate®
www.uptodate.com
@2010 UpToDate®
Liothyronine: Drug information

Pharmacodynamics/Kinetics
Onset of action: 2-4 hours
Peak response: 2-3 days
Absorption: Oral: Well absorbed (95% in 4 hours)
Half-life elimination: 2.5 days
Excretion: Urine

================================================== ==

Methylprednisolone: Drug information

Pharmacodynam ics / Ki netics
Onset of action:
Peak effect (route dependent): Oral: 1-2 hours; I.M.: 4-8 days;
Intraarticular:
1 week; methylprednisolone sodium succinate is highly soluble and has a
rapid effect by I.M. and t.V. routes

Duration (route dependent):
Oral: 30-36 hours; I.M.: 1-4 weeks; Intra-articular: 1-5
weeks; methylprednisolone acetate has a low solubility and has a sustained I.M. effect

Distribution: Vd: 0.7-1.5 L/kg

Half-life elimination: 3-3.5 hours; reduced in obese

Excretion: Clearance: Reduced in obese

............................................


http://www.endocrineweb.com/tests.html

http://www.endocrineweb.com/TFT.html
much higher top range for FT3

Free Triiodothyronine l FT3 230-619 pg/d
------------------------------------------

[JanSz]

http://www.thyroid-info.com/articles/ray-peat.htm


Increased T3 will immediately increase the conversion of cholesterol to progesterone and bile acids.

....

TRH stimulates prolactin release,

...

I have been told that the company which now owns the Armour name and manufactures "Armour thyroid USP" has added a polymer to the formula, and I think this would account for the stories I have heard about its apparent inactivity. Some people have found that the tablets passed through their intestine undigested, so I think it's advisable to crush or powder the tablets.

....


Mary Shomon: Do you think the majority of people with hypothyroidism get too much or too little iodine? Should people with hypothyroidism add more iodine, like kelp, seaweeds, etc.?

Dr. Ray Peat: 30 years ago, it was found that people in the US were getting about ten times more iodine than they needed. In the mountains of Mexico and in the Andes, and in a few other remote places, iodine deficiency still exists. Kelp and other sources of excess iodine can suppress the thyroid, so they definitely shouldn't be used to treat hypothyroidism.

JanSz-comment, I am not sure that we should stop eating iodine.
I keep eating it.
Looking for comments/arguments.
Iodine supports not only thyroid (I guess, what esle it is doing???)

..

[Massa]

Dr. Ray Peat: 30 years ago, it was found that people in the US were getting about ten times more iodine than they needed. In the mountains of Mexico and in the Andes, and in a few other remote places, iodine deficiency still exists. Kelp and other sources of excess iodine can suppress the thyroid, so they definitely shouldn't be used to treat hypothyroidism.

JanSz-comment, I am not sure that we should stop eating iodine.
I keep eating it.
Looking for comments/arguments.
Iodine supports not only thyroid (I guess, what esle it is doing???)

..
I have been digging into that before and Peat is right that supplementing iodine to iodine-sufficient subjects has been shown to INDUCE hypothyroidism. But do we know we really get enough iodine, by simply eating the few mcg we are supposed to need?
Dr. Ronald Roth, who runs a highly informative website (acu-cell.com) on vitamin/mineral balances writes:

I have tested individuals who have been ingesting as much as 6 mg (40x the RDA / RDI) of organic iodine for
longer periods of time, yet without experiencing any ill effects, so toxicity - at least for most people, and when
not using inorganic iodine - does not appear to be a major issue. However, too much iodine can trigger both,
hyperthyroidism, and in some cases hypothyroidism with all its undesirable consequences, while during
pregnancy, too much - just like too little iodine - can have adverse effects on the baby also. Supplementing
normal (RDA / RDI), or even lower amounts of iodine following long-standing iodine deficiency can trigger
hyperthyroidism in some instances.

There also seems to be an opposition of tin/iodine, where tin supports the adrenals, while iodine supports the thyroid. About tin, Dr. Roth writes:

Comparing thousands of patient records since the mid 70's showed that better than 90% exhibited below-
normal levels of tin when referenced to the status of all other essential trace minerals, making it the most
deficient element compared to any other trace mineral measured. Symptoms associated with low levels of
tin typically include depression and/or fatigue, and others.

I had 285 individuals taking part in evaluating tin, some on a short-term basis (about 3 weeks), and others
on a long-term basis (1 - 2+ years), resulting in some valuable feedback on various responses encountered,
including side effects, although the poor absorption of stannous oxide was a limiting factor in being able to
achieve optimal increases of cellular tin in all subjects.

Of those who experienced changes after supplementing tin, negative reactions, e.g. stomach / digestive
upsets, or skin reactions were at par, or less compared to the best tolerated trace minerals such as calcium,
chromium, or magnesium. Positive health effects were numerous and included improvements with fatigue,
and some forms of depression, with a general increase in energy, well-being and mood. There were also
benefits with certain types of headaches, insomnia, asthma, or improvements with digestion, skin, or various
aches and pains.

[Dr. John Crisler]

work on D1 enzyme and RT3 will take care of itself. no?
In a nutshell, yes.

[Dr. John Crisler]

Unlikely, because deiodinase D1 doesn't act specifically to boost any one of the thyroid hormone fractions.

Ie: deiodinase D1 simply boosts several thyroid hormone conversions:

..T4 -> T3
..T4 -> rT3
..T3 -> 3,3T2
rT3 -> 3,3T2

(diagram here)
http://en.wikipedia.org/wiki/File:Iodothyronine_deiodinase.pngThis needs a bit of refining.

D1=T4->T3
D3=T4->rT3 but also T3->T2 (double whammy)

[Dr. John Crisler]

Very nice, Jan!
To my list of tests, on post #44
http://anabolicminds.com/forum/male-anti-aging/66268-jans-bloodtest-april13-2.html

I have added:

27 ------------ T3, Total (859X)
28 ------------ T4, Total (Thyroxine)
================================================== =======

so Wilson’s syndrome
• Ratio of T3/RT3 < 10:1

could be loked at and evaluated.
-------------------------------------------------------------------------
http://www.ehealthspan.com/download/4-Thyroid1.1.doc
RT3 and cellular metabolism

• RT3 decreases cellular energy production
• T3 reverses this decline


• Okamoto R et al. Adverse effects of reverse triiodothyronine on cellular metabolism as assessed by 1H and 31P NMR spectroscopy. Res Exp Med (Berl) 1997;197(4):211-7
Low T3 , high RT3 predicts mortality
• Surviving patients improved the T3/RT3 ratio
• Sick euthyroid syndrome

• Schulte C et al. Low T3-syndrome and nutritional status as prognostic factors in patients undergoing bone marrow transplantation.
Bone Marrow Transplant 1998 Dec;22(12):1171-8
Thyroid and Ankylosing Spondylitis
• FT4, FT3 and TT3 were significantly lower
• TSH and TT4 were found to be in the normal range
• rT3 was significantly increased.
• The prevalence of anti-thyroid antibodies was significantly higher in the AS-group.


• Lange U et al. Thyroid disorders in female patients with ankylosing spondylitis.
Eur J Med Res 1999 Nov 22;4(11):468-74


Selenium supplementation and thyroid
• Critically ill patients
• 500 mcg Seleneium, 150 mg alpha tocopherol, 13 mg zinc
• Normalization of TT3. TT4 and RT3 with improvement in T3/RT3 ratio with selenium
• No chance with alpha tocopherol or zinc (JanSz note, I think dr ment change not chance)

• Berger MM et al. Influence of selenium supplements on the post-traumatic alterations of the thyroid axis: a placebo-controlled trial. Intensive Care Med 2001 Jan;27(1):91-100
Thyroid and regaining lost weight after dieting
• T3/RT3 falls during acute and chronic calorie restriction
• Is this a factor why lost weight is usually regained?

• Weinsier RL et al. Do adaptive changes in metabolic rate favor weight regain in weight-reduced individuals? An examination of the set-point theory. Am J Clin Nutr 2000 Nov;72(5):1088-94
Anti-Aging Medicine
Thyroid replacement therapy
Wilson’s reverse T3 dominance syndrome
• Stress….Increased Cortisol….Impaired T4 to T3 conversion….increased RT3 conversion
• RT3 occupies binding sites of T3, impairs T4 to T3 conversion and may feed back to decrease TSH
• “Hypometabolism” produced which decreases enzyme activity in all systems…
• Fatigue, headache, migraine, PMS, irritability, fluid retention, anxiety and panic attacks, hair loss, depression, decreased memory and concentration, low sex drive, unhealthy nails, low motivation and ambition
• No references to Wilson’s syndrome on medline
Wilson’s syndrome• Ratio of T3/RT3 < 10:1
• Low body temp
• Symptoms
Treatment – Wilson’s syndrome
• Compounded extended release T3 7.5 mcg q12 hours x 2 days
• If oral temp not 98.2 increase to 15 mcg q 12 hours x 2 days
• Increase till 98.2 or symptoms of thyroid excess
• Then taper back at same rate
• Then temp should stay normal or another cycle required

[Dr. John Crisler]

For $20 I can buy this presentation.
Most likely it is very much related to dr Ron Rothenberg's notes I posted link to, above.

Looks like dr Rothenberg believe in Wilson’s syndrome
and how to treat it.
The thing is, we are on dr John's board
waiting for his blessing or other details.
Dr John, rules.
================================================== ========
Less than 2 months ago.

http://www.prolibraries.com/a4m/?select=session&sessionID=1801
PC07b - Thyroid Replacement Therapy
$20.00 Purchase Conference: A4M Las Vegas 2008
Speaker: Ronald Rothenberg, MD
Date/Time: December 11, 2008 8:45 am - 9:30 am
Length: 30m 54s - 68 Slides

================================================== ========
http://www.prolibraries.com/a4m/?select=session&sessionID=1524
PC04c - Thyroid Hormone
$20.00 Purchase Conference: A4M Washington DC 2008
Speaker: Ron Rothenberg, MD
Date/Time: July 17, 2008 9:20 am - 10:00 am
Length: 40m 09s - 98 Slides
================================================== ========

http://www.prolibraries.com/a4m/?select=session&sessionID=1309
PC01c - Thyroid Hormone Deficiency - Diagnostic and Treatment T3, T4, THS
$20.00 Purchase Conference: A4M Orlando 2008
Speaker: Ron Rothenberg, M.D.
Date/Time: April 25, 2008 12:00 am - 12:00 am
Length: 46m 44s - 97 Slides
================================================== ========Dr. Rothenberg is, IMPO, the finest Anti-Aging doctor in the world. He's also a really great guy. We had a great time having lunch together in a small restaurant in Mexico City in January. His Spanish fluency was a great help, too (also could tell me what it was I was eating LOL).

I introduced him to Bill Faloon, owner of LEF, in Orlando a few weeks ago.

[Dr. John Crisler]

Some of BigPharma links;

Merck Manual
Euthyroid Sick Syndrome
http://www.merck.com/mmpe/sec12/ch152/ch152c.html
http://www.merck.com/mmpe/sec12/ch152/ch152c.html?qt=Euthyroid%20Sick%20Syndrome&alt=sh

Treatment

Treatment with thyroid hormone replacement is not appropriate. When the underlying disorder is treated, results of thyroid tests normalize.

This is CLEAR BIG-PHARMAs response.
You just go ahead and try to find the "underlying disorder", good f**ken luck.
------------------------------------------------------------

emedicine.medscape
Euthyroid Sick Syndrome

The effects of nonthyroidal illness
Triiodothyronine and reverse triiodothyronine

http://emedicine.medscape.com/article/118651-overview
------------
Euthyroid Sick Syndrome: Multimedia
http://emedicine.medscape.com/article/118651-media

Conditions that affect thyroid function tests
Laboratory Studies
http://emedicine.medscape.com/article/118651-diagnosis

-----------------------
http://emedicine.medscape.com/article/118651-treatment
Medical Care
There is no prospective study to date demonstrating benefit or harm of thyroid hormone replacement in NTI. Thyroid hormones have been used in the setting of NTI in various settings with T4 and T3 replacement and still remain controversial. Dr De Groot has supported the notion that nonthyroidal illness syndrome is a manifestation of hypothalamic-pituitary dysfunction, and in view of current evidence, he proposed that treatment should be considered with appropriate replacement therapies such as pituitary hormones, hypothalamic factors in addition to thyroid hormones.The problem is when you pump more T4 in, you also then get more rT3. This is why you MUST give even more T3 as well.

[Dr. John Crisler]

Finally.

I think I've found the best solution - and this guy is a medical professional - a pharmacist - in Australia (of all places)

http://www.custommedicine.com.au/blog/2007/04/17/reverse-t3-dominance/

Hiis conlcusion (bottom of page) is:

"We have found that by using a consistent low dose of T3 over two to three months without the need of cycling the dose, as described by Dr Wilson, in addition to addressing the causes of improper T4 metabolism, many patients have responded favorably with improved symptoms and a reduction in reverse T3 levels."

The statement about addressing the causes of improper T4 metabolism is mentioned a little further up the document, ie:

"In addition nutrients such as selenium, zinc, Vit B6, B12 and E, iron and iodine should be supplemented as they are necessary cofactors for the proper conversion of T4 into T3."

I think this gent has the solution.I'm with these guys.

The problem with treating per Dr. Wilson's protocol is it doesn't really focus on runnng T4 through D1. THAT is what is necessary to affect a return to health. Feed the bear (D1)!

[Dr. John Crisler]

One down, so many to go.

In vicinity of the 2-3 months period, when planning to start tappering back, it would be good to know the desirable levels of important thyroid analytes, so one is able to make sure that he reached planned end point of theraphy.
================================================== ==================

I am not confortable with
http://www.custommedicine.com.au/blog/2007/04/17/reverse-t3-dominance/
explanation of ratio, namely this:
"Ideally the ratio of T3/rT3 multiplied by 100 should be between 1.06 to 1.13. "
Working with any numbers requires careful watching units.
Better example would help.
Those numbers would not work if we use results from Quest Diagnostics.
Untill we know the units used above we cannot use their condition to figure out RT3 dominance
-----
But using Quest Diagnostics units would work if we use condition for RT3 dominance as done by dr Rothenberg (post #4 & #9 this thread)
hes wrote the condition as:

Wilson’s syndrome
• Ratio of T3/RT3 < 10:1
----------------------
Quest Diagnostics reports like this:

T3,Total (60-181) ng/dL
T3, Reverse (11-32) ng/dL
--------------------

at lower range the ratio is
60/11~6
at higer range the ratio is
181/32~6

someone with RT3 at high range RT3~32
and T3 at low range T3~60
would have this analytes within normal range, but

would have ratio 60/32~2 less than 10, and would have Wilson's syndrome

Basically dr Rothenberg is saying that we need to have 10x or more of T3 relative to RT3 to avoid RT3 dominance..
================================================== =================

("Wilson's Syndrome" - also known as Multiple Enzyme Dysfunction or MED)It's a situation of competitive inhibition.

But I do not consider ratios as treatment goals. Rather, they are useful for describing/explaining current state of health.

[Dr. John Crisler]

If people are truly getting results with this program, that is certainly proof of its validity. At least for a portion of the patient population--it sure seems like there is a lot of "it wasn't done right" going on; but granted, this hormonal stuff can be VERY challenging.

These points of science remain:

rT3 has a very short half-life, about 3 hrs. Therefore it does not "build-up" in tissue, or need "clearing".

Supplementing pure T3 (even appropriately as sustained release preparation) does nothing for increasing enzyme D1 activity-and this is the whole problem. D3 is dominating over D1, and so rT3 is being produced antagonistically over T3. Precisely, it's the T4 run through D1 to become T3 that makes the difference. Supplemented T3 does not do this. Picking up D1 acitivity, specifically D1/D3, that is the cure.

I simply have not seen Armour Thyroid increase rT3 as this protocol directly states. And I monitor same. But perhaps it's the other things I am concurrently doing in these patients that is making the difference.

I also do not wish to ramp up heart rate to tachycardic rate as will happen with many by hypersupplementing T3 only.

Again, D1 is the centerpiece of thyroid optiminization.I need to correct myself here.

Adding T3 indeed makes one healthier, and so does foster increased D1 activity. However, you need more T4 coming through D1 to achieve your goals. Inasmuch as adding T4 while in the diseased state also shnts more into rT3, this can be a two-edged sword.

THIS is where clinical experience comes in.

[Dr. John Crisler]

Of note, due to the short half-life of T3, ANY T3 supplementation can be described as "cycling".

I know I'm a geek, but I find that kind of funny.



That's not wholly true. Wilson's therapy specifically cycles the dose of T3 from low, to too high and back to low again.

This is a critical aspect of Wilson's therapy. It must not be overlooked.

HOWEVER, if someone chooses to supplement with pure T3 without cycling, in order to achieve the same end result - then that is not Wilson therapy. That is "someone else's therapy".

Let's be very clear about this.

Cycling T3 = Wilson Therapy
Constant dose of T3 = someone else's therapy




Again, this statement completely misses the cyclic part.

Therefore this is not describing Wilson's therapy. This is describing "someone else's therapy".

[JanSz]

Quote:
Originally Posted by wondering
work on D1 enzyme and RT3 will take care of itself. no?


In a nutshell, yes.

It was a polite exchange and gives one sense of direction.

It would help to get details of what is meant by "working on D1 enazyme".

At this time, my definition of working on D1 enzyme is,
correcting deficiencies identified by these tests:

Spectracell-5000
all micronutrients and lipids

Essential & Metabolic Fatty Acids Analysis (EMFA)
Hair Analysis


Lets leave aside any overkill part.
Lets concentrate what is still missing?


..

[josh]

Reading the last pages leaves my head swimming.

Perhaps I need to step back and evaluate my 50mcg daily of T3?

[JanSz]

Reading the last pages leaves my head swimming.

Perhaps I need to step back and evaluate my 50mcg daily of T3?

50mcg-T3/day + 100mcg-T4/day

is average (first approximation) replacement dose
replacement means that TSH is expected to be suppressed down to zero in most people

obviously
it (the dose) should be tweaked via testing
it should be used only after basic investigation and support of adrenals and thyroid is in place

but
off hand I do not see much wrong with 50mcg-T3/day

....

From pdf on post #193 above:

U.S, Brand Names Cytomel®; Triostat®

Hypothyroidism: Oral: 25 mcg/day increase by 12.5-25 mcg/day every 1-2 weeks to a
maximum of 100 mcg/day; usual maintenance dose: 25-75 mcg/day

/////////////////

[JanSz]

Of note, due to the short half-life of T3, ANY T3 supplementation can be described as "cycling".

I know I'm a geek, but I find that kind of funny.

Short half life of T3 is repeated often.

Once here:
http://webcache.googleusercontent.com/search?q=cache:7oYbXg_4IqMJ:www.musclechatroom.com/forum/archive/index.php/t-1211.html+Liothyronine+half+life+T3+site:musclecha troom.com/forum/&cd=1&hl=en&ct=clnk&gl=us

Dr. John Crisler
05-22-2008, 01:22 PM

"or take SR T3. It has a half-life of 7 hours."

----------------
Yet
http://en.wikipedia.org/wiki/Liothyronine_sodium

Half life 2.5 days
-----

http://musclechatroom.com/forum/showpost.php?p=87050&postcount=193
Onset of action: 2-4 hours
Peak response: 2-3 days
Absorption: Oral: Well absorbed (95% in 4 hours)
Half-life elimination: 2.5 days

---------------------------------------------

How to reconcile this?

When I am late with taking my next 25mcg-T3 I note temperature drop,
so I am tending to believe in 7 hours,
but
I feel that little discussion would help.

..

[chilln]

Short half life of T3 is repeated often.

Once here:
http://webcache.googleusercontent.com/search?q=cache:7oYbXg_4IqMJ:www.musclechatroom.com/forum/archive/index.php/t-1211.html+Liothyronine+half+life+T3+site:musclecha troom.com/forum/&cd=1&hl=en&ct=clnk&gl=us

Dr. John Crisler
05-22-2008, 01:22 PM

"or take SR T3. It has a half-life of 7 hours."

----------------
Yet
http://en.wikipedia.org/wiki/Liothyronine_sodium

Half life 2.5 days
-----

http://musclechatroom.com/forum/showpost.php?p=87050&postcount=193
Onset of action: 2-4 hours
Peak response: 2-3 days
Absorption: Oral: Well absorbed (95% in 4 hours)
Half-life elimination: 2.5 days

---------------------------------------------

How to reconcile this?

When I am late with taking my next 25mcg-T3 I note temperature drop,
so I am tending to believe in 7 hours,
but
I feel that little discussion would help.

..

The reason why measuring body tempoerature is not a useful indicator of any specific thyroid hormone, is because the body has temperature compensation mechanisms built in which use sweat (evaporation), thermal radiation, and sugar burn.

Attempting to monitor thyroid hormone T3 metabolism via body temperature measurements if guaranteed to be unreliable until you can completely remove, or compensate for, the effects of these three cooling and warming systems.

It takes far more technology than we can muster in 2010 to measure and correctly account for the effects of these thermal compensation mechanisms, in order to attrubute a change in temperature to a reasonably precise level of thyroid hormone T3.

.

[JanSz]

IODINE

http://www.iodine4health.com/index.htm

-------
IODINE AND THE THYROID

http://www.iodine4health.com/body/thyroid/thyroid.htm
---------------------
EFFECTS OF IODINE DEFICIENCY ON THE THYROID

http://www.iodine4health.com/body/thyroid/thyroid_iodine_deficiency.htm

-----------------------
EFFECTS OF IODINE EXCESS ON THE THYROID

http://www.iodine4health.com/body/thyroid/excess/excess.htm

Excess iodide inhibits TPO-catalyzed iodination.
Iodination is inhibited if iodide concentrations are greater than 1 mM. Excess iodide may also result in a decrease in TPO genetic expression.
--------------------------------------------------------------
Thyroid peroxidase (TPO) is an enzyme made in the thyroid gland that is important in the production of thyroid hormone. TPO is found in thyroid follicle cells where it converts the thyroid hormone T4 to T3.

================================================== ===
IODINE AND AUTOIMMUNE ISSUES

http://iodine4health.com/disease/thyroidisease/autoimmune/autoimmune.htm

the antibodies attack the thyroid peroxidase (TPO) and thyroglobulin (Tg), two essential components essential in the synthesis of thyroid hormones. Thus, over time, there tends to be a decreased production of thyroid hormones, or hypothyroidism
---------------------------------

REPRINTED FROM WWW.THYROIDMANAGER.ORG
Chapter 8 – Hashimoto’s Thyroiditis

http://www.thyroidmanager.org/Chapter8/chapter8.pdf

----------------------------------
ORTHOIODOSUPPLEMENTATION
http://iodine4health.com/ortho/ortho.htm

TRADITIONAL VIEW.
The traditionalists see the RDA of approximately 150 mcg per day as appropriate and necessary. Amounts above 1 mg (1000 mcg) would be seen as excessive and potentially toxic. And the primary criterion for determining excess would be thyroid function, especially increases in TSH (Thyroid Stimulating Hormone, a common blood test used to measure thyroid function).

From this point of view, the traditionalists view most Americans as getting sufficient iodine from their daily diets, and the primary concern is Iodine Toxicity, which requires being careful that people do not consume too much iodine.

ORTHOIODOSUPPLEMENTATION VIEW.
In contrast, the Orthoiodosupplementation point of view sees the RDA as too low, with 6.5 - 12.5 mg of iodine seen as necessary for total body health for most people. Amounts of iodine up to 50 mg (and sometimes more) may be necessary for brief periods of time to restore iodine sufficiency.



//

[JanSz]

http://www.bprcem.com/article/S1521-690X(09)00074-8/abstract

Volume 23, Issue 6, Pages 769-780 (December 2009)



Thyroid function is modulated by genetic and environmental causes as well as other illnesses and medications such as gonadal or sex steroids. The latter class of drugs (sex steroids) modulates thyroid function. Gonadal steroids exert their influence on thyroid function primarily by altering the clearance of thyroxine-binding globulin (TBG). While oestrogen administration causes an increase in serum TBG concentration, androgen therapy results in a decrease in this binding protein. These effects of gonadal steroids on TBG clearance and concentration are modulated by the chemical structure of the steroid being used, its dose and the route of administration. Despite the gonadal steroids-induced changes in serum TBG concentrations, subjects with normal thyroid glands maintain clinical and biochemical euthyroidism without changes in their serum free thyroxine (T4) or thyroid-stimulating hormone (TSH) levels. In contrast, the administration of gonadal steroids to patients with thyroid diseases causes significant biochemical and clinical alterations requiring changes in the doses of thyroid medications. Similarly, gonadal steroid therapy might unmask thyroid illness in previously undiagnosed subjects. It would be prudent to assess thyroid function in subjects with thyroid disease 6–8 weeks after gonadal steroid administration or withdrawal.


===============================

Increasing TT

reduces SHBG
reduces TBG

what is does to CBG (cortisol binding globulin)

does it really influences Albumin??

SHBG, TBG, CBG

[JanSz]

http://www.definitivemind.com/forums/showpost.php?p=3298&postcount=6


O.K. I agree. It was a poor choice of words.

If I did not know the person and just have labs, then I would suspect thyroid hormone signaling is not working well if one or more of the following is present in an adult:

Total T4 < 8.0 ug/dL
Total T3 < 100 ng/dL (this varies)
Free T3 < 340 pg/dL
Free T4 < 1.2 ng/dL
TSH > 2.0 uIU/mL (this varies depending on the presence of metabolic problems. Also, if the goal of treatment is optimization, then this criteria is tightened so that a TSH > 1.0 would be suspect for suboptimal thyroid signaling).

Whether or not to add thyroid hormone depends on several factors.

This is where obtaining the necessary information via history, physical exam, and other lab tests is important.

For example, if Total T4 is between 8.0 to 12.0 (this range is shifted upwards in women who take birth control), then I would hesitate to add more thyroid hormone. The reason is that there is sufficient thyroid hormone to activate and do it signaling job. If the person shows signs and symptoms of hypothyroidism, but adequate T4, then it is not thyroid hormone production that is the problem but what happens to the thyroid hormone after it is released.

For example, under some circumstances, such as infection, more T4 becomes converted to Reverse T3 than usual. This would then lead to a loss of T3 production and symptoms and signs of hypothyroidism. Adding T3 is an option. Some people respond to T3, with subsequent reduction of Reverse T3 production and normalization of thyroid hormone activation. In some people, however, T3 can also increase inflammatory signaling in the immune system, causing the situation to worsen. T3 may then be not tolerable due to occurrence of palpitations. The best solution would be to investigated further to determine why T4 is becoming converted more so to Reverse T3 then treat the cause, such as infection. Once the cause is determined and treated, thyroid activation to T3 can return.

If Free T3 is low but T4 is normal, then additional questions include: are thyroid binding proteins elevated? For example, if a person is taking birth control pills or if the person has excess estrogen production, then estrogen signaling is elevated. This triggers thyroid binding globulin production from the liver. TBG then binds to thyroid hormones, reducing the free levels of thyroid hormone, causing then a relative state of hypothyroidism.

If T3 is low and T4 is sufficient, then conversion of T4 to T3 is suspect. Questions to ask then include: is there sufficient deiodinase enzyme production to do the conversion? Is there sufficient selenium to make these enzymes? Is there sufficent norepinephrine signaling to trigger deiodinase enzyme production? Is there impaired liver function? etc. etc.

If T4, Free T4 and Free T3 are sufficient, yet TSH is elevated, then the questions include: Is there a problem in transporting thyroid hormone past the blood brain barrier so that it can do its work in the brain? Are there nutritional deficiencies (such as with vitamin A, iron, etc.) which are impairing thyroid signaling? Determining the questions to ask as to why thyroid hormone is not working and determining solutions to the problem would be the better answer, not just adding more thyroid hormone.

Etc. Etc. Etc.

Despite having thyroid test results, there is a lot more information that needs to be obtained to determine whether or not one should add thyroid hormone.

If the physician is confident and wants to dive in to do thyroid replacement, in a clinical trial, to see if it is beneficial, then he or she can do so after doing a risk assessment for the intervention.

There is a lot of complexity underneath the surface of what seemingly is a simple treatment.

Often more data is necessary to help determine risk prior to even a clinical trial of thyroid hormone.



////

[4aminsomniac]

Of note, due to the short half-life of T3, ANY T3 supplementation can be described as "cycling".

I know I'm a geek, but I find that kind of funny.

I have seen many medical professionals claim T3 has a short half-life. Some claiming 7-8hrs, but I have never seen anybody prove this.

The Cytomel prescribing info document, and everything else I can find shows the half-life as 2-2.5/days.

If that is the case, I don't see why a TR T3 or multiple dosing per day is necessary.

Compared to T4, I would say T3 has a relative short half-life.

[4aminsomniac]

Something I haven't seen in this thread is what are the typical symptoms of high RT3?

Same as hypo?

[PureChance]

RT3 blocks T3 = typical hypothyroidism symptoms even with good free T3 numbers

[4aminsomniac]

RT3 blocks T3 = typical hypothyroidism symptoms even with good free T3 numbers

So, even having a supressed TSH of .2, top of level Free T3, Mid Free T4 level, and over the top RT3, hypo symptoms.

Ideas for treating this scenario? I've read all sorts of things, 1) keep some T4 synthetic going in, add more syn T3; 2) Straight T3 no T4 as Wilson's suggest, ramp up after two days and watch temperature, ramp back down; 3) Long term low dose Syn T3 and no Syn T4 and see how you feel etc...

For my stated scenario, how would one go about addressing it? TSH supressed, Free T3 at top, RT3 at Top, Free T4 mid range? Currently Syn T4 and Syn T3 combo being used, and not in huge amounts. I'm a good converter, but obviously in a bad way too.

[PureChance]

http://www.thyroid-rt3.com/

this site seems to have some good information from what I can tell.

or stopthethyroidmadness.com

[JanSz]

So, even having a supressed TSH of .2, top of level Free T3, Mid Free T4 level, and over the top RT3, hypo symptoms.

Ideas for treating this scenario? I've read all sorts of things, 1) keep some T4 synthetic going in, add more syn T3; 2) Straight T3 no T4 as Wilson's suggest, ramp up after two days and watch temperature, ramp back down; 3) Long term low dose Syn T3 and no Syn T4 and see how you feel etc...

For my stated scenario, how would one go about addressing it? TSH supressed, Free T3 at top, RT3 at Top, Free T4 mid range? Currently Syn T4 and Syn T3 combo being used, and not in huge amounts. I'm a good converter, but obviously in a bad way too.

iron deficiency, as indicated by an iron saturation below 25 or a ferritin below 70 ///http://nahypothyroidism.org/deiodinases/ [[[[[ http://findarticles.com/p/articles/mi_m0FDN/is_4_5/ai_65068470/
T4-only preparations should not be considered optimal thyroid replacement in the presence of high or high-normal reverse T3 levels (197-201) while T3 can be significantly beneficial
Do not use natural thyroid hormones (containing T4 + T3) or outright T4 when RT3>197 pg/ml=19.7ng/dL
-----------------------
High RT3=fire
adding T4=gasoline

.................

[saltimbanc0]

Free copy of the manual for treating high rt3 - apologies if its already posted in this thread somewhere.

http://www.wilsonstemperaturesyndrome.com/eManual/

How quickly do you up the doses or did you take it to find you got temperatures up?

Im at 100mcg (2 x 50 per day) and am the same as when i was running 100mcg t4 temp wise and i dont feel any more/less energy (ie i feel none)

[JanSz]

http://www.dynamicchiropractic.com/mpacms/dc/article.php?id=45537

T3 and Chronic Fatigue

By John Lowe, MA, DC
Dynamic Chiropractic – December 19, 1990, Vol. 08, Issue 26
================================================== =======

Nice logic on how stress progresses, sometimes to the point where body can't recover.

stress--->excess amount of stress hormones-->less T3 more RT3

Supplying T3 may break the viscous cycle.
----

Dr Love should have mentioned that when body stops or slows converting
T4---->T3

it does that by increasing RT3 production

----------

Forced supply of T3,
reduces stress
restores balance

................

Question
how long to wait and see if body is able to deal with stress on its own?

Current medical practice of waiting with T3 supplementation until patient is in ICU (on a death bed) begs for improvement.


///
Note
eventually person ends up unable to produce enough stress hormones
but
their RT3 remains high

double whammy.

/////////

[rfish1966]

iron deficiency, as indicated by an iron saturation below 25 or a ferritin below 70 ///http://nahypothyroidism.org/deiodinases/ [[[[[ http://findarticles.com/p/articles/mi_m0FDN/is_4_5/ai_65068470/
T4-only preparations should not be considered optimal thyroid replacement in the presence of high or high-normal reverse T3 levels (197-201) while T3 can be significantly beneficial
Do not use natural thyroid hormones (containing T4 + T3) or outright T4 when RT3>197 pg/ml=19.7ng/dL
-----------------------
High RT3=fire
adding T4=gasoline

.................

heh like a ferritin of 9 ; )

[JanSz]

heh like a ferritin of 9 ; )

http://musclechatroom.com/forum/showpost.php?p=115539&postcount=99

Do not wait too long,

go see hematologist PRONTO


///

[4aminsomniac]

iron deficiency, as indicated by an iron saturation below 25 or a ferritin below 70 ///http://nahypothyroidism.org/deiodinases/ [[[[[ http://findarticles.com/p/articles/mi_m0FDN/is_4_5/ai_65068470/
T4-only preparations should not be considered optimal thyroid replacement in the presence of high or high-normal reverse T3 levels (197-201) while T3 can be significantly beneficial
Do not use natural thyroid hormones (containing T4 + T3) or outright T4 when RT3>197 pg/ml=19.7ng/dL
-----------------------
High RT3=fire
adding T4=gasoline

.................



What do you make of this then? I donated blood about 3 months ago or so.

[JanSz]

http://musclechatroom.com/forum/showpost.php?p=116752&postcount=21




here is an article blurb that supports the idea that RT3 itself interfers with T4 to T3 conversion.

http://www.holtorfmed.com/index.php?section=downloads&file_id=17


Endocrinology;101(2):453-63
A study of extrathyroidal conversion of thyroxine (T4)
to 3,3’,5-triiodothyronine (T3) in vitro.
Most endocrinologists believe that reverse T3 (3,3’,5-triodothyronine) is just and inactive metabolite with no physiologic effect. This is an erroneous belief, however.
This and other studies demonstrate that reverse T3 (rT3) is a more potent inhibitor
of T4 to T3 conversion than PTU (propylthiouracil), which is a medication used to decrease thyroid function in hyperthyroidism. In fact, rT3 is 100 times more potent than PTU at reducing T4 to T3 conversion. Clearly demonstrating that rT3 not just an inactive metabolite, but rather an potent inhibitor of tissue thyroid levels. The authors conclude, “Reverse t3 appeared to inhibit the conversion of t4 to T3 with a potency which is about 100 times more than PTU…”

[TryingToFix]

Peripheral metabolism of thyroid hormones: a review.
Kelly GS.

http://www.thorne.com/altmedrev/.fulltext/5/4/306.pdf

This article talks much about what has been discussed in the thread. Further talking about the liver function in the RT3 process.

[chilln]

Peripheral metabolism of thyroid hormones: a review.
Kelly GS.

http://www.thorne.com/altmedrev/.fulltext/5/4/306.pdf

This article talks much about what has been discussed in the thread. Further talking about the liver function in the RT3 process.

This article only lists one association between thyroid hormones and cortisol, which is that excess cortisol causes low T3.

This article overlooked the most important conclusion regarding thyroid hormones T4, T3, reverse T3 and cortisol, which is that too low cortisol results in a downregulation of D1 enzymes, reducing the rate of conversion of T4 into T3, and thus too low cortisol is statistically the most likely cause for high RT3, because too low cortisol is highly prevalent in modern society.

By missing the most critical association between thyroid hormones T4, T3 and reverse T3 and cortisol, this article is therefore very very misleading, and this article should only be considered for the info it contains about hormones other than reverse T3.

.

[JanSz]

This article only lists one association between thyroid hormones and cortisol, which is that excess cortisol causes low T3.

This article overlooked the most important conclusion regarding thyroid hormones T4, T3, reverse T3 and cortisol, which is that too low cortisol results in a downregulation of D1 enzymes, reducing the rate of conversion of T4 into T3, and thus too low cortisol is statistically the most likely cause for high RT3, because too low cortisol is highly prevalent in modern society.

By missing the most critical association between thyroid hormones T4, T3 and reverse T3 and cortisol, this article is therefore very very misleading, and this article should only be considered for the info it contains about hormones other than reverse T3.

.

Good catch, thank you.

Specially useful when presented as a simple Cause and Effect analysis.

///

Side question

when presented with high RT3
specially high RT3 that persists over years
should one keep attempting to lower it in natural way (vitamins, minerals, micronutrients, HC, pregnenolone, progesterone, phophatidylserine(tweaks), similar....)
or
in more direct way
starving body of T4 by supplying some excess of T3 over long time?



///
What is better for long term health
high RT3 plus hope that one gets better and the RT3 will subside naturally
forced reduction of RT3 by using T3 ?


/////

[4aminsomniac]

This article only lists one association between thyroid hormones and cortisol, which is that excess cortisol causes low T3.

This article overlooked the most important conclusion regarding thyroid hormones T4, T3, reverse T3 and cortisol, which is that too low cortisol results in a downregulation of D1 enzymes, reducing the rate of conversion of T4 into T3, and thus too low cortisol is statistically the most likely cause for high RT3, because too low cortisol is highly prevalent in modern society.

By missing the most critical association between thyroid hormones T4, T3 and reverse T3 and cortisol, this article is therefore very very misleading, and this article should only be considered for the info it contains about hormones other than reverse T3.

.

I would have to lean towards this as many people's issues.

I recently added just about 1.2mg-2.5mg/day of hydrocortisone, it seems to help with my RT3 problems and I have a clearer head, increased energy, and my temperature is raising up.

I am going to stop the hydrocortisone and do a saliva 4x test again, but my last saliva test 2.5yrs ago showed low across the entire day. Just riding above the bottom line. So adding just a touch of hydrocortisone, can go a long way it seems.

[mcs5309]

Good catch, thank you.

Specially useful when presented as a simple Cause and Effect analysis.

///

Side question

when presented with high RT3
specially high RT3 that persists over years
should one keep attempting to lower it in natural way (vitamins, minerals, micronutrients, HC, pregnenolone, progesterone, phophatidylserine(tweaks), similar....)
or
in more direct way
starving body of T4 by supplying some excess of T3 over long time?



///
What is better for long term health
high RT3 plus hope that one gets better and the RT3 will subside naturally
forced reduction of RT3 by using T3 ?


/////

I think hitting it on both ends is the key (e.g., adequate levels of ferritin and Vit A + forcing exogenous T3). I am using SRT3 and increasing 10mcg/week to pulse and temp tolerance (I just bumped to 50mcg/day). I am now iron (ferrous glycinate 50mg BID) and Vit A (20KIU) loading until tissue saturation which will take some time, as my ferritin level was under 70, and according to Dr. Mariano, needs to be at 150-200 ng/ml, otherwise, thyroid hormone is incapable of working. He also feels that HC is an incomplete treatment approach and too much causes cell death + you lose other hormone signals.

[spiderRico]

I would have to lean towards this as many people's issues.

I recently added just about 1.2mg-2.5mg/day of hydrocortisone, it seems to help with my RT3 problems and I have a clearer head, increased energy, and my temperature is raising up.

I am going to stop the hydrocortisone and do a saliva 4x test again, but my last saliva test 2.5yrs ago showed low across the entire day. Just riding above the bottom line. So adding just a touch of hydrocortisone, can go a long way it seems.

are you saying you only do 1.2-2.5 mg/day or are you saying you bumped up your dose from whatever it was by 1.2-2.5 mg/day.

That would be a really, really low dose.

Do you have labs showing a lowering of rt3? Or are you just going from symptoms?

[JanSz]

I think hitting it on both ends is the key (e.g., adequate levels of ferritin and Vit A + forcing exogenous T3). I am using SRT3 and increasing 10mcg/week to pulse and temp tolerance (I just bumped to 50mcg/day). I am now iron (ferrous glycinate 50mg BID) and Vit A (20KIU) loading until tissue saturation which will take some time, as my ferritin level was under 70, and according to Dr. Mariano, needs to be at 150-200 ng/ml, otherwise, thyroid hormone is incapable of working. He also feels that HC is an incomplete treatment approach and too much causes cell death + you lose other hormone signals.

Hitting both ends is for you or me.
Actually hitting cortisol end first and T3 when you RT3 is stubborn.
But, what if you have to argue with someone who is totally against using T3 only.
How to present argument to convince.

================================================== ===

At one time I had
ferritin=28
Hbg=16

using iron pills I raised to
ferritin=35
Hbg=16

then I went on UNILiver

ferritin=82
Hbg=16.8

Problem is shortly after my Hgb went up to 17.5

I had to do phleblotomy.


I asked my doctor about how to raise ferritin without raising Hgb.
Got no answer.

If you have a chance asking dr mariano I would appreciate.
Send me PM with answer if you get it.

//

[hardasnails1973]

rt 3 is very over rated and by treating is directly with even amounts of t3 10-15 mcgs are driving shbg up the ass. I have seen personally and also in patients shbg go from 30 to 75 in just matter of a few months. Treating the thyroid even with minimal dosage of t-3 is throwing the some peoples adrenals into crazy tail spin. Again every one is different, but this is occuring why to nuts. Any one preaching >18-20 ft3:rt3 should have their head examined. Peoples libido are taking a nose dive and all that was added was t-3 and shbg doubled. If you want solution with t3 then danazol needs to be added to offset the change to shbg from thyroid. Problem solved..

[phife]

rt 3 is very over rated and by treating is directly with even amounts of t3 10-15 mcgs are driving shbg up the ass. I have seen personally and also in patients shbg go from 30 to 75 in just matter of a few months. Treating the thyroid even with minimal dosage of t-3 is throwing the some peoples adrenals into crazy tail spin. Again every one is different, but this is occuring why to nuts. Any one preaching >18-20 ft3:rt3 should have their head examined. Peoples libido are taking a nose dive and all that was added was t-3 and shbg doubled. If you want solution with t3 then danazol needs to be added to offset the change to shbg from thyroid. Problem solved..

So then what do you suggest? I have a very high RT3 along with low free T3 and high-normal free T4. There is so much contrasting advice that my head is beginning to spin. My doc put me on some T3 in addition to my Synthroid and I feel 100x worse. I don't know where else to turn.

[hardasnails1973]

So then what do you suggest? I have a very high RT3 along with low free T3 and high-normal free T4. There is so much contrasting advice that my head is beginning to spin. My doc put me on some T3 in addition to my Synthroid and I feel 100x worse. I don't know where else to turn.

Work on finding out the reason WHY. I have seen alot of heavy metals and also cortisol issues with t4 to t3 conversions.

[phife]

Work on finding out the reason WHY. I have seen alot of heavy metals and also cortisol issues with t4 to t3 conversions.

My salivary cortisol test looks decent enough.

How would I test for heavy metals?

Would low TIBC/UIBC and high ferritin interfere with conversion?

[chilln]

I think hitting it on both ends is the key (e.g., adequate levels of ferritin and Vit A + forcing exogenous T3). I am using SRT3 and increasing 10mcg/week to pulse and temp tolerance (I just bumped to 50mcg/day). I am now iron (ferrous glycinate 50mg BID) and Vit A (20KIU) loading until tissue saturation which will take some time, as my ferritin level was under 70, and according to Dr. Mariano, needs to be at 150-200 ng/ml, otherwise, thyroid hormone is incapable of working.


I doubt that our bodies need anything to "tissue saturation" levels.

I suspect this is a workaround solution, but as such I don't agree with it. I don't agree with any workaround solution which overdrives anything to such a high degree.

I don't even agree with super high dosages of Iodine to overdrive T4 -> T3 conversion, because the best way to drive T4 -> T3 conversion (in preference to T4 -> reverse T3) is to use the following simple sequential process:


1a) ensure adequate selenium and iodone and vitamin D, not to "overdrive" levels.
1b) monitor improvement in T4 -> T3 conversion, versus T4 -> reverse T3 conversion.

2a) ensure plenty of pregnenolone <-- citical
2b) confirm adequate cortisol (due to pregnenolone boost) <-- citical
2c) monitor improvement in T4 -> T3 conversion, versus T4 -> reverse T3 conversion.

PREGENOLONE IS CRITICAL TO ENSURE ADEQUATE NEUROTRANSMITTERS TO ENSURE THE BRAIN CAN MANAGE THE MONITORING OF METABOLISM FUNCTIONS AND CAN COORDINATE D1 ENZYME ACTIVITY IN PERIPHERAL TISSUES

CORTISOL IS CRITICAL BECAUSE THYROID HORMONE T3 AND CORTISOL WORK SYNERGISTICALLY TO CREATE THE BOOST IN METABOLISM WHICH IS INCORRECTLY ATTRIBUTED TO THYROID HOROMONE T3 ALONE

3a) If thyroid hormone antibodies are low, then boost T4 if the body refuses to produce enough T4, but only to the extent where the body will convert it into T3 (not reverse T3)
3b) monitor improvement in T4 -> T3 conversion, versus T4 -> reverse T3 conversion.

4a) boost T3 directly to make up the remaining T3 needed to ensure optimum metabolism.
4b) monitor improvement in T4 -> T3 conversion, versus T4 -> reverse T3 conversion.



He also feels that HC is an incomplete treatment approach and too much causes cell death + you lose other hormone signals.


When too low cortisol is as a result if too low ACTH, then the solution is to boost pregnenolone, because ACTH controls the rate of synthesis of pregnenolone from LDL cholseterol.

Since too-low-ACTH is the statistically most likely cause for too low cortisol, therefore supplementing with pregnenolone is going to be the statistically most likely and affordable solution to workaround too-low-ACTH.

.

[chilln]

So then what do you suggest?


see my above post. Its explains thyroid hormone management very simply, and it applies to you too.



I have a very high RT3 along with low free T3 and high-normal free T4. There is so much contrasting advice that my head is beginning to spin.


see my above post. Its explains thyroid hormone management very simply, and it applies to you too.

You're getting contrasting / conflicting info re thyroid hormone management because the vast majority of medical professional advisers and researchers are simply unaware that thyroid hormone T3 and cortisol work synergistically to produce the increase in metabolism which is incorrectly attributed to thyroid hormone T3 alone.

.

[phife]

is a serum blood draw the best way to measure selenium and iodine?

[chilln]

If you want solution with t3 then danazol needs to be added to offset the change to shbg from thyroid. Problem solved..


But this solution doesn't address the more fundamental problem of too low cortisol.

The fact that a person's thryoid hormone metabolism is too low, and that an increase in T3 (due to supplementtion) results in an increase in SHBG, is due to the following feedback loops:

1) cortisol is initially too low
2) thryoid hormone metabolism is too low because cortisol is too low
3) testosterone metabolism is upregulated because cortisol metabolism is too low
at this point cortisol should be boosted, but is overlooked
4) at this point T3 is boosted via supplemetary means:
...a) increases serum T3
...b) further reduces cortisol
5) reduction in cortisol further increases T metabolism, even if serum T levels don't change
6) increase in T metabolism is countered in some people by an increase in SHBG
7) at this point danazol is introduced to reduce SHBG, which boosts bioavailable T, but T metabolism doesn't need a boost, even though T serum levels are seen to have reduced.

###

The solution in this person's case is to boost cortisol right from the start, and then the boost in T3 will not cause in increase in SHBG.

Note that boosting cortisol will probably also require an increase in supplementary T dosage because cortisol naturally downregulates T metabolism.

.

[Massa]

rt 3 is very over rated and by treating is directly with even amounts of t3 10-15 mcgs are driving shbg up the ass. I have seen personally and also in patients shbg go from 30 to 75 in just matter of a few months. Treating the thyroid even with minimal dosage of t-3 is throwing the some peoples adrenals into crazy tail spin. Again every one is different, but this is occuring why to nuts. Any one preaching >18-20 ft3:rt3 should have their head examined. Peoples libido are taking a nose dive and all that was added was t-3 and shbg doubled. If you want solution with t3 then danazol needs to be added to offset the change to shbg from thyroid. Problem solved..

looking at the study below, I suppose your patients were women?

Exp Clin Endocrinol Diabetes. 1995;103(5):339-42.
Age modulates effects of thyroid dysfunction on sex hormone binding globulin (SHBG) levels.

Lecomte P, Lecureuil N, Lecureuil M, Osorio Salazar C, Valat C.

CHRU Bretonneau, France.
Abstract

Symptoms of thyroid dysfunction are difficult to detect in elderly people and TSH is sometimes unreliable. We therefore tested the value of SHBG as a marker of thyroid hormone action on the liver to determine the thyroid status of elderly people. Aging euthyroid men and women have a significant increase in SHBG (p > 0.0001). In aging women the decrease in SHBG with hypothyroidism and increase with hyperthyroidism are highly significant (p < 0.0001 and p < 0.0005 respectively). No significant variation in SHBG was observed in men with thyroid dysfunction. SHBG can help to determine the thyroid status of aging women.

PMID: 8536064 [PubMed - indexed for MEDLINE]

edit: I just found numerous studies that indicate this effect can be observed in men, as well. sorry!

[Massa]

here is some more data:
J Clin Endocrinol Metab. 1988 Apr;66(4):740-6.
Sex hormone-binding globulin in the diagnosis of peripheral tissue resistance to thyroid hormone: the value of changes after short term triiodothyronine administration.

Sarne DH, Refetoff S, Rosenfield RL, Farriaux JP.

Department of Medicine, University of Chicago, Illinois 60637.
Abstract

Thyroid hormone is one of several factors that modulate the level of sex hormone-binding globulin (SHBG) in serum. SHBG levels are usually elevated in thyrotoxicosis and have been reported to be normal in a few patients with generalized resistance to thyroid hormone (GRTH). This study was designed to determine whether basal serum SHBG levels or the SHBG response to short term T3 administration could be used as an index of thyroid hormone action and thus serve as a test for the evaluation of patients suspected of having peripheral tissue resistance to thyroid hormone. Serum SHBG, total T4, free T4 index (FT4I), total T3, and TSH levels were measured in 21 normal subjects, 28 hypothyroid patients, 20 thyrotoxic patients, and 10 patients with GRTH. Excluding patients with GRTH, serum basal SHBG values were correlated with FT4I values (r = 0.66; P less than 0.0001). Mean SHBG levels in the patients with GRTH [37.6 +/- 16.2 (+/- SD) nmol/L] were not significantly different from those in the normal subjects (35.1 +/- 19.3 nmol/L) or hypothyroid patients (26.3 +/- 17.1 nmol/L), but were significantly lower than those in the thyrotoxic group (64.7 +/- 19.2 nmol/L; P less than 0.001). All 10 patients with GRTH had basal SHBG values in the normal range, but 7 of 20 (35%) thyrotoxic patients also had normal basal SHBG values. T3 was given orally for three sequential 3-day periods at doses of 50, 100, and 200 micrograms daily to 7 normal subjects, 11 hypothyroid and 3 thyrotoxic patients, and all 10 patients with GRTH. The serum SHBG concentration was measured on the last day at each dosage level. During T3 administration, SHBG levels increased in all individuals with normal tissue responsiveness. The increase above the basal value (delta SHBG) at each T3 dose was similar in normal, hypothyroid, and thyrotoxic individuals (non-resistant subjects). After administration of 50 micrograms T3 daily, the mean delta SHBG level was decreased [-2.9 +/- 5.3 (+/- SD) nmol/L] in the resistant patients and increased (4.0 +/- 4.9 nmol/L; P less than 0.005) in the nonresistant subjects. After administration of 100 micrograms T3 daily, the mean delta SHBG was -4.5 +/- 6.8 nmol/L in the resistant patients and 8.6 +/- 5.1 nmol/L (P less than 0.0001) in the nonresistant subjects. Serum SHBG decreased by more than 2 nmol/L in 6 of 10 (60%) resistant patients, but in no nonresistant subject.(ABSTRACT TRUNCATED AT 400 WORDS)

PMID: 3346353 [PubMed - indexed for MEDLINE]

[Massa]

here is another pretty interesting study, showing the effect of high T3 on CBG


Eur J Endocrinol. 1995 May;132(5):594-8.
Opposite effects of thyroid hormones on binding proteins for steroid hormones (sex hormone-binding globulin and corticosteroid-binding globulin) in humans.

Dumoulin SC, Perret BP, Bennet AP, Caron PJ.

Department of Endocrinology, CHU Rangueil, Toulouse, France.

Erratum in:

* Eur J Endocrinol 1995 Sep;133(3):381.

Abstract

Sex hormone-binding globulin (SHBG) and corticosteroid-binding globulin (CBG) levels were evaluated in euthyroid (N = 111), hyper- (N = 58) and hypothyroid (N = 38) men, in pre- and postmenopausal women (study 1) and in hyper- (N = 24) and hypothyroid (N = 15) patients before and after treatment with carbimazole or levothyroxine therapy (study 2). The SHBG levels are increased in hyper- and decreased in hypothyroid patients, whereas CBG levels are increased in hypo- and decreased in hyperthyroid patients. The SHBG levels are higher in women than in men with similar thyroid status. Plasma SHBG levels are correlated positively whereas CBG levels are correlated negatively with free thyroid hormone concentrations in men as well as women. In hypothyroid patients, SHBG concentrations increased (p < 0.01) and CBG concentrations decreased (p < 0.01) during levothyroxine treatment. In hyperthyroid patients, SHBG concentrations decreased (p < 0.01) and CBG concentrations increased (p < 0.01) during antithyroid treatment. The SHBG and CBG concentrations in treated hypo- and hyperthyroid patients were not significantly different from those of euthyroid controls. Our data indicate that SHBG and CBG levels depend on thyroid status. Corticosteroid-binding globulin is an index of thyroid hormone action at the liver level whose changes are opposite to those of SHBG in hyper- and hypothyroidism.

PMID: 7749500 [PubMed - indexed for MEDLINE]

[hardasnails1973]

looking at the study below, I suppose your patients were women?


edit: I just found numerous studies that indicate this effect can be observed in men, as well. sorry!

More so it was men with issues with e2 issues

Chillin,
Even raising cortisol in these cases did not help and the adrenals where supported with cortef before adding the t3. Adrenal saliva where completely normal as well as there were no digestion issues in many cases I have encountered with no low cortisol symptoms. t-3 has to have some effect on the liver pathways that makes it increase SHBG. Mine, Pmgamer, brando shbg went up even while being on cortef prior before.

[pmgamer18]

I for one have higher RT3 levels and for the life of me can't get a grip on this FT3/RT3 ratio thing. My Free T3 is 3 pg/ml. my RT3 is 41 range is 11 to 32 ng/dl the ratio I think is 7.3.

My RT3 went up after having Heart Bypass Surgery now two yrs later it's high because I am on a lot of pain from being on Statin Drugs. My pain is so bad I can't stand up without help or walk with out a walker.

I am on 150 mcs of Synthroid doing T3 only 5mcg 3x's a day. I feel better on this then I did on 4 grains for Amour.

There is no way I can stop my Synthroid and take huge doses of T3 only meds. I am just off the top of being hyper taking T3 only 3xs a day at the low dose of 5 mcgs.

My fix for my RT3 is to keep my Cortisol levels supported on 30 mgs a day of Cortef and keeping my T levels up into the upper 1/3 of my labs range and holding down my E2 levels. Once I get my Co Q10 levels back up from Statin Drug damage I feel my RT3 will come down but I don't feel bad from my levels of RT3.

It's like Chilln says fix your hormones and let the rest fall in place.

[chilln]

More so it was men with issues with e2 issues

Chillin,
Even raising cortisol in these cases did not help and the adrenals where supported with cortef before adding the t3. Adrenal saliva where completely normal as well as there were no digestion issues in many cases I have encountered with no low cortisol symptoms. t-3 has to have some effect on the liver pathways that makes it increase SHBG. Mine, Pmgamer, brando shbg went up even while being on cortef prior before.


I know that a high percentage of people experience ACTH suppression from even low doses of HC / Cortef (eg: 10mg) and should not take more than 5mg of HC / Cortef at a time, yet as a result, these people must take 5 mg of HC / Cortef approx every 1.5 to 2 hours to keep their coritsol levels adequately high without ACTH suppression.

I suspect you, pmgamer18 and brando are in this group too.

What happens to these people is that they absorb HC / Cortef very quickly, as a result each dose of HC / Cortef higher than 5mg suppresses ACTH for longer than the boost from the HC / Cortef lasts. So the average cortisol is not consitently high, but rather it's high - then too low - then high - then too low - then high - then too low.

However, switching from HC to transdermal pregnenolone results in consistently high cortisol, which downregulates T metabolism effectively, and then boosting thyroid hormone T3 boosts metabolism (including T metabolism) but since cortisol keeps T metabolism in check therefore SHBG doesn't rise (because the body doesn't need to downregulate T metabolism any further)

We've all been underestimating how much cortisol our bodies need, and we haven't been monitoring the inconsistent delivery of cortisol from HC / Cortef in those members who absorb it very quickly.

.

[phife]

However, switching from HC to transdermal pregnenolone results in consistently high cortisol, which downregulates T metabolism effectively, and then boosting thyroid hormone T3 boosts metabolism (including T metabolism) but since cortisol keeps T metabolism in check therefore SHBG doesn't rise (because the body doesn't need to downregulate T metabolism any further)



For someone NOT on testosterone replacement...what are the ramifications of boosting cortisol which then downregulates T metabolism?

[JanSz]

Time HC dose, mg
8 ------- 10 ------- 5
9 ------- ------- 5
10 ------- -------
11 ------- 10 ------- 5
12 ------- -------
13 ------- ------- 5
14 ------- -------
15 ------- 5 ------- 5
16 ------- -------
17 ------- -------
18 ------- 5 ------- 5
19 ------- -------
20 ------- -------
21 ------- -------
22 ------- -------
23 ------- 5 ------- 5
24 ------- -------
1 ------- -------
35 35

[chilln]

More so it was men with issues with e2 issues

Chillin,
Even raising cortisol in these cases did not help and the adrenals where supported with cortef before adding the t3. Adrenal saliva where completely normal as well as there were no digestion issues in many cases I have encountered with no low cortisol symptoms. t-3 has to have some effect on the liver pathways that makes it increase SHBG. Mine, Pmgamer, brando shbg went up even while being on cortef prior before.


Looks like you were wrong about Phil's SHBG. I had to move that discussion to a different thread because it was no longer on topic, ie:

http://musclechatroom.com/forum/showthread.php?t=15384

I do believe your own SHBG does indeed increase with thyroid hormone supps, and therefore the info I published about this phenomenon (addressed to Phil) definintely does apply to you because your body type needs higher-than-average cortisol.

ie: the boost to your SHBG comes from the fact that your thyroid boosts your metabolism, including your testosterone metabolism, but your body is detecting too high testosterone metabolism, and so has to downregulate your testosterone, so your body boosts SHBG to soak up the excess T metabolism.

I'll spell it out:
1) your cortisol is too low, but not dangerously low, even though you're supplementing with HC / Cortef,
2) your testosterone metabolism is upregulated because your cortisol too low (normal response),
3) you then add some thyroid hormone T3 which boosts your overall metabolism (normal response)
4) the boost to your overall metabolism from T3, also boosts your T metabolism (normal response)
5) your body detects that your T metabolism is too high, so it cranks up your SHBG (normal response for those people where it occurs, not all people respond in this way)
6) the increase in SHBG reduces your T metabolism back to your body's genetic setpoint for optimum T (normal response).

###

While the above info wasn't applicable to Phil, it is applicable to you.

.

[pmgamer18]

Yep this about covers it I have told him I feel he needs more HC.

Looks like you were wrong about Phil's SHBG. I had to move that discussion to a different thread because it was no longer on topic, ie:

http://musclechatroom.com/forum/showthread.php?t=15384

I do believe your own SHBG does indeed increase with thyroid hormone supps, and therefore the info I published about this phenomenon (addressed to Phil) definintely does apply to you because your body type needs higher-than-average cortisol.

ie: the boost to your SHBG comes from the fact that your thyroid boosts your metabolism, including your testosterone metabolism, but your body is detecting too high testosterone metabolism, and so has to downregulate your testosterone, so your body boosts SHBG to soak up the excess T metabolism.

I'll spell it out:
1) your cortisol is too low, but not dangerously low, even though you're supplementing with HC / Cortef,
2) your testosterone metabolism is upregulated because your cortisol too low (normal response),
3) you then add some thyroid hormone T3 which boosts your overall metabolism (normal response)
4) the boost to your overall metabolism from T3, also boosts your T metabolism (normal response)
5) your body detects that your T metabolism is too high, so it cranks up your SHBG (normal response for those people where it occurs, not all people respond in this way)
6) the increase in SHBG reduces your T metabolism back to your body's genetic setpoint for optimum T (normal response).

###

While the above info wasn't applicable to Phil, it is applicable to you.

.

[TryingToFix]

Why does it seem like that if the morning cortisol/adrenal level is not supported adequately (through whatever means) that fatigue/lethargy carries through the entire day even if additional support at other times of the day is increased?