Re: There's something I just don't understand

[Guest guest]

I do feel there si a place for T4. Whnen I have been on T3 only if I

miss A dose by an hour I could feel it, God forbid I go to work withotu

my pill box! On Armoru skipping a day;s meds never bothered me but tiny

bit,that was because I had T 4oin my body to convert as well as it

could. I have never been a real great converter. BUT the reason I am

going back to Armour has NOTHING to do wiht T4, it has everything to do

with Calcitonin. NO synthetic thyrodi med contains this hormone which

helps keep calcium in your bones. Mostly it is destroyed by stomach

acids but taking Armour (or other natural thyroid) sublingually I am

gettign the benefit of calcitonin. So people do not seem to process T3

well. Some have sensitive systems due to low ferritin or low or high

cortils that make T3 be utilized at an unnatural rate. But ANYONE that

has a tendency to high RT3 should clear it out wiht a straight T3 till

ti is normal and the cause of their high RT3 is cleared. If they do not

I have seen peole go all the way to 10 grains of Amrour and sitll have

hy0o sympotms and weight that they cannot lose. BUT you need to keep in

mind that HIGH thyroid doses are no better than low. If you take too

much T3 or Armour or T4 it will cause you to have the same (or quite

simi,ar) symptoms as low thyroid will. lack of energy, muscular and

joint pain and weight probems even fluid retention. Then you may also

have problems with Insulin resistance which thyroid cannto totllay

control that may make the weight stay on. Sex hormones even play a

strong role in this too!

--

Artistic Grooming- Hurricane WV

http://www.stopthethyroidmadness.com/

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

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

[Guest guest]

Hi ,

You know how high Estrogen will trigger SHBG to bind and escort it out of

the body? Well ....what if the same happens with thyroid. Could RT3 go up

from having high free T3.....as long as there's enough T4 around to make

it from? That way the body could regulate its set point of how much Free

T3 we were programmed to have in our blood. If that were true my

tiny amount of T4 is being tapped to make RT3 b/c my body sees my T3 as

too high (Tho it's only slightly above the top of the range.) That would

explain why my T4 keeps getting lower (its at bottom of rnormal

ange).

I heard a rumor that Calcitonin has been taken out of Armour...is

this true?

At 05:06 PM 2/26/2008, you wrote:

I do feel there si a place for

T4. Whnen I have been on T3 only if I

miss A dose by an hour I could feel it, God forbid I go to work withotu

my pill box! On Armoru skipping a day;s meds never bothered me but tiny

bit,that was because I had T 4oin my body to convert as well as it

could. I have never been a real great converter. BUT the reason I am

going back to Armour has NOTHING to do wiht T4, it has everything to do

with Calcitonin. NO synthetic thyrodi med contains this hormone which

helps keep calcium in your bones. Mostly it is destroyed by stomach

acids but taking Armour (or other natural thyroid) sublingually I am

gettign the benefit of calcitonin. So people do not seem to process T3

well. Some have sensitive systems due to low ferritin or low or high

cortils that make T3 be utilized at an unnatural rate. But ANYONE that

has a tendency to high RT3 should clear it out wiht a straight T3 till

ti is normal and the cause of their high RT3 is cleared. If they do not

I have seen peole go all the way to 10 grains of Amrour and sitll have

hy0o sympotms and weight that they cannot lose. BUT you need to keep in

mind that HIGH thyroid doses are no better than low. If you take too

much T3 or Armour or T4 it will cause you to have the same (or quite

simi,ar) symptoms as low thyroid will. lack of energy, muscular and

joint pain and weight probems even fluid retention. Then you may also

have problems with Insulin resistance which thyroid cannto totllay

control that may make the weight stay on. Sex hormones even play a

strong role in this too!

--

Artistic Grooming- Hurricane WV

http://www.stopthethyroidmadness.com/

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

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

[Guest guest]

>>You know how high Estrogen will trigger SHBG to bind and escort it

out of the body? Well ....what if the same happens with thyroid. Could

RT3 go up from having high free T3.....as long as there's enough T4

around to make it from? That way the body could regulate its set point

of how much Free T3 we were programmed to have in our blood. If that

were true my tiny amount of T4 is being tapped to make RT3 b/c my body

sees my T3 as too high (Tho it's only slightly above the top of the

range.) That would explain why my T4 keeps getting lower (its at bottom

of rnormal ange).<<

HIgh Free T3 with low T4 si usually a cortisol issue. LOW cortisol.

Though I would think if your free T3 was WAY to high it could also

trigger the body to make T4 ionto RT3 but where is th e HIGH T3 coming

from then?

>>I heard a rumor that Calcitonin has been taken out of Armour...is

this true?<<

UNTRUE! I have contacted Forrest before about this very subject. NOTHING

that is in the pig's thyroid at slaughter is removed except fats.

--

Artistic Grooming- Hurricane WV

http://www.stopthethyroidmadness.com/

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

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

[Guest guest]

richkare@... wrote:

> My question is: Why do people need T4 at

> all? And if T4 is necessary, then why don't the " pure " T3 people have

> symptoms of a T4 deficiency????? Blood levels of Free T4 in people on

> Cytomel only must be way below the normal range.

>

Mine are. My free T4 (blood) was .63 (range .80-1.80). And I had

" normal " range antibodies. So I'm getting the results I need to have and

I really don't think I need T4, if I get optimal on T3 only. The only

reason I hope to eventually go back on Armour or thyroid-S is for the

calcitonin. Of course, new information on T4 may come to light.

> If T4 is merely a " storage hormone " and timed release/ frequent T3

> dosing can render it unnecessary, then why should people on Armour/

> Cytomel with Low Free T4 try to raise their T4 levels?????

>

Beats me. I'm NOT trying to increase my T4 levels, as I think I may have

RT3 issues, or may have had a problem with RT3. I'm going to stay on T3

until I feel optimized, then a while longer, then try to gradually go

back to dessicated thyroid. That is the plan anyway. Perhaps I will end

up on some dessicate thyroid with some T3. Time will tell.

> I wonder if some problems people have on T3 only are from an absence

> of T4, not always a low or high cortisol level. Could it be that it's

> more than a storage hormone? That due to some internal balancing

> system, low thyroxine triggers other hormones to freak out?

>

I have read that there is some suspicion that T4 does have some other

use than just as the storage thyroid hormone, but don't think there is

any actual proof as yet. The T4 only docs would have a fit at my low T4

probably.

sol

[Guest guest]

The main rumor I hear abotu the body needing T4 is that the brain needs

it to convert to T3. This was believed to be fact that T3 did nto cross

the blood/brian barrier for many years and has been disproved. T3 has a

differnt carrier protein that takes it to the brain separately from T4.

--

Artistic Grooming- Hurricane WV

http://www.stopthethyroidmadness.com/

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

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

[Guest guest]

Hi ,

Can you really be hyper if you have low-normal temps, normal blood

pressure and pulse, no diarrhea, no tremors, no overheating,...just

weight gain and fatigue? I just don't know...it seems like if I were on

too much thyroid I'd have SOME of the classic symptoms of

hyper!!

Maybe I have cancer or aids or something really over the top!!!

My female doctor told me I should just endure whatever I'm dealing with

b/c it's " probably just menopause " . She's really nice but just

clueless....only 35 or so. She has a great bedside manner but no answers.

It's hard when even well meaning docs can't help.

At 05:06 PM 2/26/2008, you wrote:

I do feel there si a place for

T4. Whnen I have been on T3 only if I

miss A dose by an hour I could feel it, God forbid I go to work withotu

my pill box! On Armoru skipping a day;s meds never bothered me but tiny

bit,that was because I had T 4oin my body to convert as well as it

could. I have never been a real great converter. BUT the reason I am

going back to Armour has NOTHING to do wiht T4, it has everything to do

with Calcitonin. NO synthetic thyrodi med contains this hormone which

helps keep calcium in your bones. Mostly it is destroyed by stomach

acids but taking Armour (or other natural thyroid) sublingually I am

gettign the benefit of calcitonin. So people do not seem to process T3

well. Some have sensitive systems due to low ferritin or low or high

cortils that make T3 be utilized at an unnatural rate. But ANYONE that

has a tendency to high RT3 should clear it out wiht a straight T3 till

ti is normal and the cause of their high RT3 is cleared. If they do not

I have seen peole go all the way to 10 grains of Amrour and sitll have

hy0o sympotms and weight that they cannot lose. BUT you need to keep in

mind that HIGH thyroid doses are no better than low. If you take too

much T3 or Armour or T4 it will cause you to have the same (or quite

simi,ar) symptoms as low thyroid will. lack of energy, muscular and

joint pain and weight probems even fluid retention. Then you may also

have problems with Insulin resistance which thyroid cannto totllay

control that may make the weight stay on. Sex hormones even play a

strong role in this too!

--

Artistic Grooming- Hurricane WV

http://www.stopthethyroidmadness.com/

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

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

[Guest guest]

Well my last saliva labs came back with T3 at 2.85 with top of range

1.10... I had NO symptoms of hyper! NONE! Even my pulse wasin the 80' s

to low 90's which has been normal fro me for several years now. SO yes I

thnk you can be hyper and not have any symptoms. I cannto lose weight

and have a constant fatigue that si not leaving whether the hyper is

causoing it or not it certainly wasn;lt making things better.

--

Artistic Grooming- Hurricane WV

http://www.stopthethyroidmadness.com/

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

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

[Guest guest]

Hi Val,

Interesting. Maybe the body " notices " high T3 and makes

adjustments to conserve energy. I read once that high T3 can raise SHBG.

SHBG will bind estrogen and testosterone (which we need for muscles, skin

and leanness). Low free Testosterone can make us tired ( I have low Test

even though I supplement it.)

On the other hand, what is your Free T4 level? THAT might be what your

body is reacting to, rather than the high Free T3. There may be a hidden

balance ( like we have with estrogen and progesterone) that gets thrown

off when T4 goes down too far...not the same as hyper but a different

kind of deficiency state.

At 09:27 PM 2/26/2008, you wrote:

Well my last saliva labs came

back with T3 at 2.85 with top of range

1.10... I had NO symptoms of hyper! NONE! Even my pulse wasin the 80' s

to low 90's which has been normal fro me for several years now. SO yes I

thnk you can be hyper and not have any symptoms. I cannto lose weight

and have a constant fatigue that si not leaving whether the hyper is

causoing it or not it certainly wasn;lt making things better.

--

Artistic Grooming- Hurricane WV

http://www.stopthethyroidmadness.com/

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

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

[Guest guest]

Well I might buy into the low T4 causing something we are unaware of,

but what about folks that do WONDERFUL on all T3? They are out there.

--

Artistic Grooming- Hurricane WV

http://www.stopthethyroidmadness.com/

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

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

[Guest guest]

Thanks, Val.

sol

wrote:

> The main rumor I hear abotu the body needing T4 is that the brain needs

> it to convert to T3. This was believed to be fact that T3 did nto cross

> the blood/brian barrier for many years and has been disproved. T3 has a

> differnt carrier protein that takes it to the brain separately from T4.

>

>

[Guest guest]

Hi Val,

I am stumped. really. I wonder whether " Straight T3

people " max out after a year, or if they can keep on that way

forever. Maybe they have higher levels of Estro and Testo (are younger or

take supplemental pills/creams). Maybe they don't have Hashi's. Or maybe

they have higher levels of naturally occurring T4 which won't convert due

to receptor issues .I wish I could conduct a large study comparing people

with high fT3/ low fT4, high fT4/ low fT3, and high both. Or to see

one that someone else did, goddammit!

I would be willing to switch to all T3 if I was feeling gradually better

the more T3 I was on (and the less T4). But since that's not happening

I'm still on the fence. I take 25 T3 and 2.5 armour tablets per day. For

a long time this worked out really well for me. My blood is showing lower

fT4 and a lower TSH on the same dose as always.... probably b/c my

Estrogen is going down with age. My former high E might have been

balanced out by high fT3. At that time it was good for me. but now unless

I add E or subtract thyroid it may be a problem.

We can come up with the perfect ratios, but as soon as we slip further

into meno (and beyond) everything alters and we have to experiment anew.

An endless challenge!

K

At 09:57 AM 2/27/2008, you wrote:

Well I might buy into the low T4

causing something we are unaware o

but what about folks that do WONDERFUL on all T3? They are out

there.

--

Artistic Grooming- Hurricane WV

http://www.stopthethyroidmadness.com/

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

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

[Guest guest]

I did not feel better on straight T3 until thr Armoru had been gone for

almost a MONTH. I needed all that T4 just about out of my system for the

receptors to even BEGIN to clear. At that time I was at 250mcg T3! Then

I had to reduce it FAST as I went hypo with symptoms. I lowered it to

150 and held that for abotu a month and had labs. Free T4 .26 free T3

6.2 But saliva still showed low free T3 it was still nto getting through

for about 3 more months. Then I have not had the hyper symptoms but I

can tell you my insulin resistnce went UP. Now with lowering the dose (I

am at 3 grains Armoru and only 25mcg T3 starting yetsterday my insulkin

needs are WAY down.

--

Artistic Grooming- Hurricane WV

http://www.stopthethyroidmadness.com/

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

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

[Guest guest]

" T3 has a differnt carrier protein that takes it to the brain

separately from T4. " [quoting Val]

I wonder if some people need the T4 because the carrier protein for T3

is impaired or deficient. So their brain gets hypo unless there is T4

available, which can convert to T3 once it gets across the blood-brain

barrier.

I don't usually have brain fog, but while I was on all T3, it was

severe, the worst I've ever experienced. Cognitive mush. My husband

has this frequently, poor guy.

[Guest guest]

>>I don't usually have brain fog, but while I was on all T3, it was

severe, the worst I've ever experienced. Cognitive mush. My husband

has this frequently, poor guy.<<

And were you on ENOUGH T3? Most peoel tend to think 30-50mg is enough and it

sin;t usually, well I ahev never seen ti be enough when that is all you are

taking. Not once.

--

Artistic Grooming- Hurricane WV

http://www.stopthethyroidmadness.com/

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

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

[Guest guest]

Well, that's what I'm trying to understand, actually. So I'll bump up

my message from last night, since I haven't had any replies.

Thanks for this discussion; it's a stimulating one. --

[Guest guest]

Val, do you know about other kinds of thyroid hormone binding that

aren't tested for when the free's are calculated from the totals?

I have lots of research on the so-called free t's actually being

bound in some cases - I am just like you, AND if I fast from thyroid

meds for a few days to please a stupid endo, not only do I get

massively hypo slowly, my free T3 can stay really high for more than

a week, despite the supposed short half life...

in short, this is caused by autoimmune antibodies to the thyroid

hormone itself in the cases I have found research on, there are known

antibodies to T3 and T4, so probably also to many other aspects of

this part of the axis.

here's a blurb I wrote plus references:

Monday, February 11, 2008

Never treat hypoT on free T3 without taking symptoms into account

aka - never discount the T3 auto antibodies....

Ok we all know that using the TSH to dose thyroid meds is like trying

to navigate a shopping mall using a soccer ball as a map - or maybe

even less useful.

TSH only has a useful relationship to serum thyroid hormones when all

systems are working properly, failing that, all bets are off.

As thyroid stimulating hormone is actually produced in the pituitary,

and is released in response to the body perceiving a need for more

thyroid hormone, a number of things can go wrong. The body may be in

thyroid hormone conservation mode, this can happen after a number of

years of being hypothyroid without treatment, or in the case of some,

extreme dieting can bring it on, shock etc. The pituitary may not be

unable to produce enough TSH to stimulate the thyroid gland, the body

may not sense the lack and stimulate the pituitary to produce TSH,

and you may have antibodies to the TSH itself, so the body attacks

it's own hormone, and your thyroid doesn't get stimulated.

To get around this, most forward thinking people use the free t3 test

to indicate how one should be replaced, correlating this to symptoms

for " most " people has shown that with a freeT3 in the top 1/4 of the

lab range, or just over, most hypothyroid people begin to feel well

and regain some of the life they have lost to the illness.

But what if your free T3 is at the top of the range with no cessation

of symptoms?

What if, like me, you can go for a week with no thyroid hormone

supplement, and your symptoms worsen to the point of being bedridden,

but your free T3 still shows on the top of range on a serum test

while free T4 and TSH are both below range?

T3 has a half life of up to 10 hours, so after a week, it should be

gone right?

Not neccesarily, what has been proven in case after case after case

where an elevated T3 in the presence of hypothyroid symptoms has been

evaluated, is the presence of antibodies to the T3 itself, which

causes it to become bound in the serum, unavailable to the cells

where it is needed for metabolism, causing high so called " free " T3

testing, and persistent hypothyroid symptoms.

Don't take my word for it, read the research, and DEMAND better

treatment to the cessation of symptoms, rather than just to make some

numbers on some paper look pretty.

http://www.ncbi.nlm.nih.gov/sites/entrez?

db=pubmed & uid=3224724 & cmd=showdetailview & indexed=google

[Triiodothyronine(T3) autoantibodies in a woman with nonthyroidal

disorder: a study on preparation of serum IgG fraction employing

protein A column chromatography]

[Article in Japanese]

Mizuno E, Sugenoya A, Haniuda M, Sakai R, Kameko M, Kato M, Iida F.

Department of Surgery, Shinshu University School of Medicine.

A 48-year-old non-goitrous woman, who had undergone cardiac surgery

for mitral stenosis under the extracorporeal circulation, showed high

levels of serum T3 and free T3 in a recent follow-up study, employing

antibody coated-bead RIA for T3 and -Amerlex M particle RIA for free

T3. However, other thyroid function tests (T4, free T4, TSH and TBG)

were normal. We suspected that thyroid hormone autoantibodies (THAA)

in her serum interfered with T3 and free T3 analyses. The presence of

THAA was demonstrated by the use of various procedures as follows.

Firstly, the patient's serum was directly incubated with 125I-T3 or -

T4 analog which did not bind to TBG, followed by B/F separation with

polyethyleneglycol, counting the precipitates. Secondly, after the

serum was treated with an acid-charcoal solution to remove

circulating thyroid hormone, the measurement of THAA was made as

stated above. Normal sera were used as controls. Both the non- and

acid-charcoal-treated sera showed much higher percentages of 125I-T3

analog precipitation as compared with controls. In the case of 125I-

T4 analog, there was no difference between them. In the third study,

the presence of IgG antibodies that bound T3 but not T4 was

investigated. The IgG fraction of the patient's serum was separated

employing a Protein A-Sepharose CL-4B column chromatography. Then,

the prepared IgG fraction was purified by a technique of gel

filtration chromatography (Sephacryl S 200). Non-purified and

purified-IgG fractions both revealed higher binding percentages of

125I-T3 analog than the control IgG fraction and non-IgG fraction of

the patient. Furthermore, a good dose response was observed between

the binding percentage of 125I-T3 analog and each dose of the

patient's serum or IgG fraction. From these observations, it was

clarified that this woman had anti-T3 IgG autoantibodies using a

Protein A column chromatography with confirmation of gel filtration

chromatography.

PMID: 3224724 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/pubmed/8006324?

ordinalpos=14 & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.P

ubmed_RVDocSum

Thyroid hormone autoantibodies and their implications for free

thyroid hormone measurement.

Vyas SK, Wilkin TJ.

Endocrine Section, University Medicine, Southampton General Hospital,

UK.

Thyroid hormone autoantibodies (THAA) disrupt the equilibrium between

thyroid hormones and their binding proteins. This may lead to

spurious estimations of free thyroxine (FT4) and triiodothyronine

(FT3) by radioimmunoassay (RIA). In the present study we highlight

the importance of THAA by examining the frequency of THAA in

consecutive sera sent to a routine district hospital laboratory. Over

a period of six months, sera were collected from 200 consecutive

hypothyroid, 200 hyperthyroid and seven patients whose clinical and

biochemical thyroid status were contradictory. A further 200 patients

with non-thyroid autoimmune conditions, 20 patients with insulin

autoantibodies and 100 healthy blood transfusion donors were studied.

In all sera, both effects of antigen removal on THAA detection and

where THAA were found, the effect of their removal on FT4, were

examined. The frequencies of THAA amongst hypothyroid, hyperthyroid

and non-thyroid autoimmune conditions were 7%, 1.5% and 7.5%

respectively, whilst no THAA were found in insulin autoantibody

positive patients and 100 blood transfusion donors. However, THAA

frequency was highest in those patients whose biochemical thyroid

status was widely inappropriate to clinical state (5/7 = 64%). Sera

stripped of thyroid hormones prior to THAA detection had

significantly higher antibody activity than unstripped sera (p =

0.0027 and p = 0.0123 for T3 and T4 binding respectively). Free

thyroxine levels measured by the Amerlex-M RIA kit after antibody

removal fell in all 21 THAA positive sera tested. The correlation

coefficient between antibody activity in serum with percentage fall

in FT4 was 0.79 (Spearman's Rank Correlation Test).(ABSTRACT

TRUNCATED AT 250 WORDS)

PMID: 8006324 [PubMed - indexed for MEDLINE]

http://www.clinchem.org/cgi/reprint/41/1/117

Spuriously High Concentration of Serum Free Thyroxine due to Anti-

Trilodothyronine Antibodies ,

R#{233}S maypin, 1.3 Fran#{231}oiGseasser,' s Boehn,2 and

Muriel Rondeau2 ['Inst. de Phys. Biol. (Dir. Pr. J.

Chambron), Facultd de Med., F-67085 Strasbourg Cedex, France;2 Med.

Interne A (Pr. D. Christmann), Clin. Med.

A, Hopital Central, CHRU, F-67091 Strasbourg Cedex, France; 3Author

for correspondence: Fax Tnt + 33 88 3714 97, E-mail sapin@...-

strasbg.frI

Free thyroxine (Fr4) is now frequently measured in serum by one-step

labeled antibody assays based on a Solid-Phase Antigen-Linked

Technique (SPALT) (1). In this assay the serum sample is incubated

with a large excess of triiodothyronine (T3)-coupled solid phase and

with a limited amount of labeled anti-T4 antibody. Because the solid

phase acts as a ligand of low affinity for the anti-T4 antibody,

interference from circulating anti-thyroid hormone (anti-T4 or anti-

T3) autoantibodies (THAA) is theoretically possible.

However, until now, to our knowledge, this assay was considered to be

only slightly affected by THAA (2-4).

The highest measured FT4 values (up to 35 pmol/L) could be related to

therapy with T4 (4). Nevertheless, recently we observed a very high

FT4 value (131 pmol/L) measured by a SPALT assay (Amerlex- MAB; Kodak

Clinical Diagnostics, Amersham, UK) in the serum of a hospitalized

patient with Crohn disease. This 33-year-old man was euthyroid by

clinical evaluation and by his normal thyrotropin serum concentration

(0.59 mIUIL, normal range 0.15-4.5 mIUfL) determined with BeriLux kit

(Behring, Marburg, Germany). The biological evaluation showed a

moderate hypergammaglobulinemia (17 g/L, normal range <14 g/L) with

increased IgG concentration (21.8 g/L, normal range <17 g/L). The

followed procedures were in accordance with the Helsinid Declaration

of 1975 as revised in 1983.

This patient's serum contained anti-T3 but no anti-T4 antibodies, as

identified with the technique of Allan et a!. (5) by using the analog

T3 or T4 radioactive tracer of the Amerlex-M FT3 or FT4 kits,

respectively (Kodak Clinical Diagnostics). The percentage of

radioactive T3 analog tracer precipitated by polyethylene glycol,

12%, was above normal (5% in absence of THAA) but still quite low.

The measurement of Amerlex-M FT3 remained normal ( 4.1 pmol/L,

reference range 3.7-9.2 pmol/L). Fixation of a radioactive '251-

labeled native T3 tracer on the fraction pre cipitated by

polyethylene glycol was also not very high: 7.1% (vs normal of <5% in

absence of THAA). That the free thyroidhormone concentrations were

normal was confirmed by two-step RIAs known to be unaffected by the

presence of THAA: FT4 24.8 pmol/L (normal range 9-25.7 pmol/L by

Gammacoat " ; Incstar, Stifiwater, MN); FT3 3.7 pmol/L (normal range

3.1-6.1 pmol/L by Ria-gnost; Behring). This very marked interference

in the FT4 Amerlex-MAB assay shows an interaction of anti-T3

autoantibodies with the T3 immobilized on the solid phase. This

interaction can occur in the presence of THAA of high affinity for

the T3 fixed on the solid phase; perhaps the serum of this patient

contains an antibody with a high affinity towards the T3- bridge that

is used to link the solid phase to T3. This interaction can also

occur with THAA of low affinity but of high capacity (i.e., the

ligand is present in high concentration) (4).

The prevalence of THAA seems to be low (1/2360) (2) but the frequency

of THAA is much higher in hypothyroid (7%), hyperthyroid (1.5%), and

nonthyroid autoimmune ( 7.5%) patients (6). Compared with other one-

step FT4 kits, the Amerlex-MAB assay is considered to be little

affected by THAA (4), with only one of eight Amerlex-MAB FT4 results

being higher than two-step values in the study by et al. (2).

However, users of this FT4 kit, and more generally of SPALT Fr4 kits

with a T3-coupled solid phase, should be aware that such methods can

give grossly misleading overestimates of FT., in presence of anti-T3

autoantibodies and produce a misclassification of thyroid sta tus.

Therefore, not only anti-T4 but also anti-T3 antibodies should be

suspected when a FT4 result does not correspond to the clinical state

of the patient.

References

1. Christofides ND, Sheehan CP, Midgley JEM. One-step,

labeledantibody assay for measuring free thyroxin. I. Assay

development and validation. Cliii Chem 1992;38:11-8.

2. R, Henley R, Shankland D. Concentrations of free thyroxunand

free triiodothyronine in serum of patients with thyroxinand

triiodothyronine-bindung autoantibodies. Clin Chem 1990;36: 470-3.

3. Sapin R, Gasser F, Schlienger JL, Chambron J. Analytical and

clinical evaluation of a new one-step non-analogue radioimmuno assay

for serum free thyroxin. Ear J Nucl Med 1990;17:111-5.

4. Sheehan CP, Christofides ND. One-step, labeled-antibody assay for

measuring free thyroxine. II. Performance in a multicenter trial.

Clin Chem 1992;38:19-25.

5. Allan DJ, F, Needham CA, Barron N, Wilkins TA, Midgley JEM.

Sensitive test for thyroid hormone autoantibodies in serum [Letter!.

Lancet 1982;ii:824.

6. Vyas SK, Wilkin TJ. Thyroid hormone autoantibodies and their

implications for free thyroid hormone measurement. J Endocrino!

Invest 1994;17:15-21.

http://www.clinchem.org/cgi/content/full/51/6/1071

Letters to the Editor

Falsely High Serum Free Triiodothyronine and Free Thyroxine

Concentrations Attributable to Anti-Diiodothyronine and Anti-

Triiodothyronine Antibodies

Kunihiro Iwahara1, Chizuko Tanabe1, Kozo Nishiyama2, Hiroyuki Ohashi

3 and Masato Maekawa1,a

1 Department of Laboratory Medicine

2 2nd Department of Internal Medicine and3 3rd Department of Internal

Medicine, Hamamatsu University, School of Medicine, Hamamatsu, Japan

aAddress correspondence to this author at: Department of Laboratory

Medicine, Hamamatsu University School of Medicine, 1-20-1 Handayama,

Hamamatsu, 431-3192 Japan. Fax 81-53-435-2794; e-mail mmaekawa@hama-

med.ac.jp

To the Editor:

We observed a patient with markedly increased free triiodothyronine

(FT3) and free thyroxine (FT4) concentrations measured on a Vitros

ECi analyzer (Ortho Clinical Diagnostics). The patient was a

hospitalized 42-year-old woman with lupus erythematosus who appeared

euthyroid and had normal thyroid-stimulating hormone (TSH)

concentrations (Table 1 in the Data Supplement that accompanies the

online version of this letter at

http://www.clinchem.org/content/vol51/issue6/). Thyroid peroxidase

antibody and thyroglobulin antibody were <0.3 kilounits/L, and

rheumatoid factor was < 6.0 kilounits/L. We suspected interference

from heterophilic antibodies (1 )(2), but our experiments suggested

interference from antibodies to diiodothyronine (T2), T3, or their

conjugates, as have been described (3 )(4)( 5). The procedures in

this study were in accordance with the Helsinki Declaration of 1975

and the subsequent 1996 amendments.

In contrast to results of the Vitros ECi FT3 and FT4 assays, which

use solid phases with T2 - and T3-gelatin, respectively, and labeled

sheep antibodies, FT3 and FT4 were normal by the Elecsys assays

(Roche Diagnostics), which use biotinylated antibodies in a one-step

method.

To the Vitros FT3II and FT4 assay wells we added 0.05 mL of serum

from the patient or from controls (n = 5) and 0.1 mL of diluent

[phosphate-buffered saline (PBS) containing, per liter, 2 mL of Tween

20 (Sigma) and 10 g of bovine globulin (Sigma)], and incubated them

at 37 °C for 18 min. After washing each well, we added 0.125 mL of

horseradish peroxidase-labeled goat anti-human IgG antibody conjugate

(Chemicon International. Inc.), diluted 50 000-fold in the same

diluent, and incubated the mixtures at 37 °C for 18 min. After each

well was washed, the Vitros Signal Reagent was added to the well, and

the luminescence was measured (ALOKA luminometer). The IgG fraction

of serum samples from the patient and from five control individuals

was purified with a MAbTrapTM Kit (Amersham Biosciences), and the IgG

concentration was adjusted to 4.0 g/L. The purified IgG (0.08 mL) was

incubated at 4 °C for 24 h with 0.08 mL of PBS alone or with T2, T3,

or T4 (Sigma; at 4570, 42, and 768 nmol/L, respectively) dissolved in

PBS. Each sample was mixed vigorously with 1.2 mL of polyethylene

glycol (PEG; 125 g/L), centrifuged at 2800g for 30 min, aspirated,

and washed with 1.2 mL of PEG (125 g/L). After the precipitates were

dissolved in 0.001 mol/L hydrochloric acid ( 0.04 mL) and neutralized

by equal amounts of 0.001 mol/L sodium hydroxide, T2 and T3 were

measured by the FT3 assay and T4 by the FT4 assay. The concentrations

of T2 were expressed as T3 concentrations. Each sample was analyzed

in duplicate. The ability of the purified IgG to bind T2, T3, or T 4

was defined as the difference between the FT3 or FT4 assay result and

the respective blank value and is reported as the T2 , T3, or T4

value.

The ratios of FT3 and FT4 concentrations in PEG-treated samples ( 6)

to those in untreated samples were significantly lower for the

patient than for 37 other patients (Table 1 in the online Data

Supplement); therefore, immunoglobulins in the patient's serum

interfered with both the FT3 and FT4 assays. FT3 and FT4 values in

the mixtures of serum with sheep IgG, bovine globulin, and gelatin

did not differ significantly from those in the mixtures of serum and

PBS only, suggesting that heterophilic antibodies and anti-gelatin

antibodies did not cause the high FT3 and FT4 values.

When we examined the patient's IgG binding with Vitros FT3II and FT4

assay wells, the luminescence generated by the patient's serum was

higher than that of the 5 control individuals (Table 1 in the online

Data Supplement). This suggested that the patient's IgG bound to T2-

and T3-gelatin.

The FT3 and FT4 concentrations in purified IgG and in treated samples

of purified IgG ( 6) were below the lower detection limits of the

Elecsys assays, suggesting an absence of T3 and T4 contamination in

the IgG fractions. The patient's T2 and T3 values were higher than

those of the 5 control individuals, but the T4 value was within 2 SD

of the values for the 5 controls (Table 1 in the online Data

Supplement). This finding implies that the patient's IgG interacted

with T 2 and T3 but not with T4. The cross-reactivity of the anti-T3

antibody with T2 in the Vitros FT3II assay was very low, whereas the

patient's T2 value was evidently higher than that of 5 control

individuals. We conclude that T2 was bound to the patient's IgG.

Because anti-gelatin antibodies in the patient's serum were not

recognized, we suggest that the interfering substance were antibodies

to T2 and T3. As the interfering antibodies did not interfere with

the Elecsys FT3 assay, the interfering antibody in the patient's

serum may recognize T 2 and T3 conjugates used in the Vitros ECi FT3

and FT4 assays, as reported for a labeled-antibody assay ( 7). We

suggest that this interference in the Vitros ECi FT3 and FT4 assays

arose from antibodies to T2 , T3, or their conjugates.

References

1. Fiad TM, Duffy J, McKenna TJ. Multiple spuriously abnormal thyroid

function indices due to heterophilic antibodies. Clin Endocrinol

(Oxf) 1994;41:391-395. [Medline] [Order article via Infotrieve]

2. Kricka LJ. Human anti-animal antibody interferences in

immunological assays. [Review]Clin Chem 1999;45:942-956.

[Abstract/Free Full Text]

3. Lai LC, Day JA, F, Peaston RT. Spuriously high free

thyroxine with the Amerlite MAB FT4 assay. J Clin Pathol 1994;47:181-

182. [Abstract/Free Full Text]

4. Sapin R, Gasser F, Boehn A, Rondeau M. Spuriously high

concentration of serum free thyroxine due to anti-triiodothyronine

antibodies. Clin Chem 1995;41:117-118. [Free Full Text]

5. R, Henley R, Shankland D. Concentrations of free thyroxin and

free triiodothyronine in serum of patients with thyroxin- and

triiodothyronine-binding autoantibodies. Clin Chem 1990;36:470-473.

[Abstract/Free Full Text]

6. Kuzuya H, Blix PM, Horwitz DL, Steiner DF, stein AH.

Determination of free and total insulin and C-peptide in insulin-

treated diabetics. Diabetes 1977;26:22-29. [Abstract]

7. Westerhuis LW, Venekamp WJ. Falsely high serum free thyroxine

concentration measured with Amerlite-MAB FT4. Clin Chem 1995;41:633-

634. [Free Full Text]

http://www.ncbi.nlm.nih.gov/pubmed/7535535?

ordinalpos=15 & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.P

ubmed_RVDocSum

Autoimmunity against thyroid hormones.

Sakata S.

Third Department of Internal Medicine, Gifu University School of

Medicine, Japan.

The presence of thyroid hormone autoantibodies (THAA) is a common

phenomenon. More than 270 cases have been reported by the end of 1993

involving not only thyroidal but also nonthyroidal disorders.

Clinically, THAA in a patient's serum produces variation in thyroid

hormone metabolism and, in particular, may interfere with the

radioimmunoassay (RIA) results of total or free thyroid hormone

measurements, which can cause unusually high or low values of the

hormones depending on the B/F separation method used. This in vitro

interference can give clinicians confusing information about the

patient's thyroid state. As a result, the patient may receive

inappropriate treatment from physicians who are unaware of this

disorder. The presence of THAA has been reported not only in humans

but also in dogs, chickens, and rats. In this review article,

clinical features of THAA and the mechanism of autoantibody

production are discussed.

PMID: 7535535 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/pubmed/7958106?

ordinalpos=12 & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.P

ubmed_RVDocSum

[studies on patients with a discrepancy between free thyroid hormones

and thyrotropin values]

[Article in Japanese]

Hisaoka T, Iino S, Saitoh H, Yoshimura H, Ishikawa N, Momotani N, Ito

K.

Department of Internal Medicine, Showa University Fujigaoka Hospital,

Yokohama, Japan.

Thyroid function has been almost exactly evaluated by the measurement

of serum free thyroxine (FT4), free triiodothyronine (FT3) and

thyrotropin (TSH) concentrations. However, we occasionally experience

patients who show a discrepancy between free thyroid hormones and TSH

values, and the assessment of thyroid function in such cases is

extremely difficult. Thyroid hormone autoantibodies (THAA) interfere

with radioimmunoassay (RIA) of FT4 and FT3 by giving inappropriate

values. To investigate the incidence of THAA, immune precipitation of

patients' sera after incubation with labelled T4 (125I-T4) or T3

(125I-T3) analog tracer was done in 394 patients with thyroid

diseases. 9 patients ( 2.3%) showed an increased binding of 125I-T4

or 125I-T3 analog. Heterophilic antimouse antibodies in a patient's

serum (human antimouse immunoglobulin antibodies: HAMA) can interfere

in two-site immunometric assays (IMA) using mouse monoclonal

antibodies and result in spuriously increased serum TSH

concentrations. Manufacturers now customarily add nonspecific mouse

immunoglobulins into their assay kits to absorb HAMA and prevent such

interference. This approach may not always be enough to prevent HAMA

interference in all samples. In 14 thyrotoxic patients with

inappropriately high TSH measured by an IMA kit, we measured the

levels of TSH by the further addition of mouse serum into this kit.

Their serum TSH levels were fully suppressed except for 2 patients

with a syndrome of inappropriate secretion of TSH (SITSH). The

presence of abnormal albumin in the serum also interferes with RIA of

FT4 and FT3. We experienced a female case of Graves' disease treated

with methimazole who showed an inappropriately high serum FT3

measured by an analog tracer RIA kit, whose serum FT4, FT3 and TSH

were 1.31 ng/dl, 19.3 pg/ml and 1.9 mu U/ml respectively. Although

the anti-T3 autoantibody was considered to be present initially,

immune precipitation of her serum with 125I-T3 analog tracer gave a

negative result. In order to elucidate this finding, Sephadex-G200

chromatography of her serum after incubation with 125I-T3 analog

tracer was done. Radioactivity of her serum in albumin fraction was

significantly higher than that of normal control serum to indicate

the presence of abnormal albumin in the serum. In conclusion, to

assess the thyroid function of a patient with a discrepancy between

free thyroid hormones and TSH values, it is important to consider the

presence of THAA, HAMA, or rarely, an abnormal albumin.

PMID: 7958106 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/pubmed/7556780?

ordinalpos=11 & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.P

ubmed_RVDocSum

[Three thyroid patients showing fluctuation of thyroid hormone

autoantibody titers during long-term treatment]

[Article in Japanese]

Ikekubo K, Hino M, Saiki Y, Kajikawa M, Hattori N, Ishihara T,

Moridera K, Kurahachi H.

Department of Nuclear Medicine, Kobe City General Hospital.

Development and fluctuation of thyroid hormone autoantibody (THAA)

titers were observed during long-term treatment of thyroid diseases

in three patients. The presence of THAA was noticed by spuriously

high serum free thyroid hormone levels measured with an analog tracer

RIA (Amerlex-M FT3, FT4) in all three patients. Amerlex-M FT3 or FT4

levels gradually decreased to appropriate values for the clinical

status according to the decreasing titers of THAA. Free thyroid

hormone levels with radiolabeled antibody radioassay (Amerlex-MAB

FT3, FT4) were not affected by the THAA and always reflected actual

thyroid function. Case 1 was a 46-year-old man with untreated primary

hypothyroidism. Auti-T4 autoantibody was detected in his serum. The

125I-T4 analog binding to the autoantibody (125I-T4 analog binding

ratio) gradually declined after L-T4 therapy and finally almost

disappeared two years and four months later. Amerlex-MAB FT4 level

rose to the normal range two months after T4 therapy, but TSH level

remained slightly elevated ( 5.4-13 microU/ml) for five months during

T4 therapy. The 125I-T4 analog binding ratio and anti-Tg autoantibody

(TgAb) titer were inversely correlated. Case 2 was a 72-year-old

woman had received desiccated thyroid for a long time. Sequential

changes of 125I-T4 analog binding ratio were very similar to those of

TgAb titer. Case 3 was a 74-year-old woman with Graves' disease. She

had been treated with methimazole (MMI) and desiccated thyroid for

three years and five months. Ten months after stopping both drugs,

anti-T3 autoantibody was detected. The 125I-T3 analog binding ratio

was transiently elevated and gradually declined to reference range

for four years during L-T4 therapy. 125I-T3 analog binding ratio and

TgAb titer changed in a similar way. These results suggest that

desiccated thyroid hormone therapy and TgAb formation are related to

the development of THAA and that L-T4 therapy reduces the THAA titer.

PMID: 7556780 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/pubmed/8697622?

ordinalpos=10 & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.P

ubmed_RVDocSum

Autoantibodies to thyroid hormones: the role of thyroglobulin.

Erregragui K, Cheillan F, Defoort JP, Prato S, Fert V.

Immunotech, Marseille, France.

Autoantibodies against thyroid hormones (THAA) are frequently

detected in the sera of patients with thyroid disorders together with

autoantibodies against thyroglobulin (TGAA). THAA are considered to

be a subset of TGAA, but alternative possibilities have not been

excluded. We hypothesize that if THAA arise through an immune

response to iodothyronines carried by circulating thyroglobulin

(hTg), THAA should be found together with autoantibodies against the

peptide backbone of hTg (TPAA) close to the hormone-forming sites. We

measured TPAA in 178 serum samples, obtained from healthy subjects

and patients with thyroid disorders, using two hormone-forming

peptides isolated from hTg. The occurrence of TPAA was much lower

than that of TGAA. Autoantibodies to the hormone-rich peptide, P3,

were significantly more common than autoantibodies to the hormone-

poor peptide, P1 (111/178 = 62.3% for TGAA versus 21/178 = 11.8% for

anti-P3 TPAA and 7/178 = 3.9% for anti-P1 TPAA). The presence of

autoantibodies to thyroid hormones was investigated in 25 TPAA+ and

26 TPAA- sera. THAA were found more frequently in TPAA+ sera (10/25 =

40% for TPAA+ and 4/26 = 15.3% for TPAA-). Correlation analysis shows

that the anti-P3, but not the anti-P1 binding activity, correlates

positively with the THAA-binding activity (P < 0.001 for anti-T4

THAA; P < 0.01 for anti-T3 THAA). Specificity of anti-P3 TPAA

indicates that a subset of the anti-P3 antibodies is directed against

the thyroid hormone moiety and another subset is directed against the

peptide backbone near the hormone-forming peptide, according to our

hypothesis. These results indicate that the THAA response is an anti-

hTg response directed, in a significant number of cases, against the

hormone-forming site included in the P3 peptide. This response seems

to be elicited by either native hormone-rich hTg or by hTg fragments.

PMID: 8697622 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/pubmed/9175389?

ordinalpos=9 & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pu

bmed_RVDocSum

Antitriiodothyronine antibody in patient with Hashimoto's thyroiditis.

Plengvidhya N, Sunthornthepvarakul T, Vannasaeng S.

Department of Medicine, Faculty of Medicine, Siriraj Hospital,

Mahidol University, Bangkok, Thailand.

We described a 44-year-old female patient with a history of goiter

for 2 months. Physical examination revealed a diffusely enlarged

thyroid gland weighing 40 g firm to hard in consistency. She was

clinically euthyroid and had neither ophthalmopathy nor dermopathy.

Serum thyroid hormone levels revealed total T4 (RIA) of 4.8

micrograms/dL (normal, 4-11 micrograms/dL), total T3 (RIA) of above

600 ng/dL (70-175 ng/dL), and TSH (IRMA) of 54 mU/L (0.3-6 mU/L).

Antithyroglobulin and antiperoxidase antibody titers were 1:5,120 and

1:409,260, respectively. Because of the discrepancy between the

patient's clinical status and laboratory values, assay for thyroid

hormone autoantibodies (THAA) was done and subsequently demonstrated

antitriiodothyronine antibody with percentage of precipitation by

polyethylene of 98.4 per cent (normal range, 3.06 +/- 8.58%). In

conclusion, THAA should be suspected in patients whose clinical

status is incoherent with the thyroid function test.

PMID: 9175389 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/pubmed/6896035?

ordinalpos=1 & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pu

bmed_RVAbstractPlus

[A study on anti-T3 and anti-T4 autoantibodies found in two sisters

with juvenile hypothyroidism due to Hashimoto's thyroiditis (author's

transl)]

[Article in Japanese]

Nakamura S, Fushimi K, Okuyama M, Miura K.

Anti-thyroid hormone autoantibodies were found in two sisters of

short stature (case 1: 13 years old, case 2: 10 years old). Physical

examination revealed clinical findings of hypothyroidism with diffuse

goiter. A diagnosis of Hashimoto's thyroiditis was made by open

biopsy of the thyroid gland in both patients. Serum levels of T3 and

T4 were assayed by double antibody radioimmunoassay. In case 1, serum

T3 level was 16 ng/dl and serum T4 level was 2.0 microgram/dl. In

case 2, serum T3 levels were high (range, 375 approximately 1660

ng/dl), while serum T4 remained at a very low level (0.9

microgram/dl). On the other hand, the level of T3 in case 2 as well

as the level of T4 in case 1 was not detectable by a single antibody

radioimmunoassay using dextran-coated charcoal or polyethylene glycol

separation. In each case, the serum TSH level measured by double

antibody radioimmunoassay was extremely high (255 microunits/ml in

case 1, 240 microunits/ml in case 2), which was compatible with the

clinical features of primary hypothyroidism. Sera from both patients

were incubated with 125I-T3 and 125I-T4, followed by precipitation

with polyethylene glycol. The binding of 125I-T3 with serum from case

2 and the binding of 125I-T4 with serum from case 1 were markedly

high, suggesting the presence of T3- and T4-binding substance(s) in

the sera. IgG prepared from the sera of both cases showed marked and

specific binding with T3 in case 2 and T4 in case 1. The association

constant for T4-antibody in case 1 was 5.2 x 10(8) M-1 and for T3-

antibody in case 2 was 5.0 x 10(9) M-1. The binding capacity for T4

was 1.2 ng/ml.IgG and for T3 was 0.3 ng/mg.IgG.

PMID: 6896035 [PubMed - indexed for MEDLINE]

Labels: anti T3 antibodies, free t3, hashimoto, hypothyroid,

research, symptoms, thyroid, tsh

>

> Well my last saliva labs came back with T3 at 2.85 with top of

range

> 1.10... I had NO symptoms of hyper! NONE! Even my pulse wasin the

80' s

> to low 90's which has been normal fro me for several years now. SO

yes I

> thnk you can be hyper and not have any symptoms. I cannto lose

weight

> and have a constant fatigue that si not leaving whether the hyper

is

> causoing it or not it certainly wasn;lt making things better.

>

> --

> Artistic Grooming- Hurricane WV

>

> http://www.stopthethyroidmadness.com/

>

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

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

>

[Guest guest]

Though these are a biot over my head in the general gyt of them I get

the picture. WOW.. a whole new era of thyroid problems is uncovered adn

possibly more methods to detect and HOPEFULLY treat them. Like I have

said befre, there are intrinsic factors in whole animal hormones such as

Armoru that we still do not understand and certainly are not duplicated

in symthetic hormone analogs. Iam going to run these studies by my

doctor. I actually have one I am talking wiht that I am going to see in

a few months thta may well be interested in this and certainyl will be

ebtter able to understand and interpret them to me.

--

Artistic Grooming- Hurricane WV

http://www.stopthethyroidmadness.com/

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

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

[Guest guest]

Hi Val,

Well, how do you like that, I'm on almost the same meds as you! 25

cytomel plus 2.5 Armour but maybe I'll raise it to 3. I'd be

curious to see what your new labs will be now that the insulin resistance

is gone. Maybe low T4 or high T3 eventually brings insulin

resistance.

At 10:23 AM 2/27/2008, you wrote:

I did not feel better on

straight T3 until thr Armoru had been gone for

almost a MONTH. I needed all that T4 just about out of my system for the

receptors to even BEGIN to clear. At that time I was at 250mcg T3! Then

I had to reduce it FAST as I went hypo with symptoms. I lowered it to

150 and held that for abotu a month and had labs. Free T4 .26 free T3

6.2 But saliva still showed low free T3 it was still nto getting through

for about 3 more months. Then I have not had the hyper symptoms but I

can tell you my insulin resistnce went UP. Now with lowering the dose (I

am at 3 grains Armoru and only 25mcg T3 starting yetsterday my insulkin

needs are WAY down.

--

Artistic Grooming- Hurricane WV

http://www.stopthethyroidmadness.com/

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

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