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From: B. Harris)
Subject: Re: More on iodide deficiency
Date: 13 Apr 1997

In <>
(Margie Krick) writes:

>On Sun, 13 Apr 1997 00:14:08 -0700, John Guzobad <>
>>> Most all molecles of iodine is greedily snatched from the blood stream
>>> by the gland manufacturing thyroxin. A high reserve supply can
>>> cause...
>>I thought "un-used" iodine was *excreted*, not *stored* as your "reserve
>>supply" phrase suggests.  Can you provide some references to this end ?
>For the heck of it,  I looked at random in one of the antique books on
>the CD/R full we distribute, and immediately found this;
>Iodism - A condition arising from the prolonged use of iodine , marked
>by redness of conjuction and mucus membrane of the respiratory
>passages, furry throat, and Lachrymotion................
>People were aware of this in the 1800's years. If you look around you
>should find many references to iodized iodine, etc., and the raw
>natural sources. It's out there, heck, it is probably in one of these
>antique books.

    It takes huge amounts of iodine to give you the "iodism" symptoms
noted above-- on the order of several GRAMS a day.   The doses usually
used in iodated expectorants, in other words.  There is no way it is
going to happen with iodized salt no matter how much you eat.

    There is a condition known as Basdow's disease, or "Jod-Basdow"
(Jod = Iodine in German; Count Basdow is not to be confused with Count
Basey), in which people with thyroid nodules given small amounts of
supplemental iodine become hyperthyroid.  This does pop up in a few
people in populations when iodization is started.  Epidemiologists know
that you cause a certain amount of Basdow as the price for preventing a
lot of endemic goiter.  But the first is rare, and the second is
widespread in most inland societies without supplements.

                                              Steve Harris, M.D.

From: B. Harris)
Subject: Iodine Deficiency in N. America (was: Lower Your Cholesterol Risk 
Date: 16 May 1997

In <> (Noel A.
Taylor) writes:

   >>What's wrong with a doctor knowing his/her limits is that
many don't.  This newsgroup alone thoroughly demonstrates the
mechanism whereby medical doctors assume that any training they
haven't received isn't valid.  Also demonstrated is the attitude
that if you don't have an MD, your opinion doesn't matter.  The
final nail in the coffin is that it's difficult to refer for
something you don't understand well enough to grasp the
importance of.<<


   It sure is.  As neatly illustrated by your demonstration,
below, that you know too little about the thyroid to be able to
intelligently treat OR refer people with thyroid diseases.

    Your problem is not really that medical doctors don't know
enough.  Your problem is that they know too much, since you have
some nonscientific theories about iodine deficiency, and some
voodoo method of supposedly detecting same, which you're unhappy
that physicians don't accept.  Well, my heart bleeds for you.
But if you persist in believing in nonsense, that's what you get.

   >>I join you in supporting a multidisciplinary approach to
health care, not only in "medicine" but in all of health care.  I
hope to see it someday.<<

   It will never happen so long as some members of the team
persist in believing in baloney.

   >>Example:  thyroid dysfunction is common, if the per capita
rate of synthroid prescription is any indicator.  Testing for
TSH, T3 and T4 levels is the standard of care upon which such
prescription is based:  if TSH is high and T3/T4 is low, write
that prescription!  Unfortunately, this standard of care
appears to ignore iodine deficiency as a portion of the
differential diagnosis.  Think about it. <<

    We physicians have thought about it, thank you very much.
The problem is that YOU haven't thought about it.  The standard
of medical care is that prescriptions for thyroid hormone are
written with no further workup only in very select situations.
Mainly this happens with adults (usually older women) with
persistently elevated TSH levels who have NO palpable thyroid
enlargement whatever.  This isn't the picture you see in "iodine
deficiency" (where you already have a goiter by the time T4
levels drop below normal and TSH is much elevated), rather it's
the picture you see in burned out autoimmune thyroiditis.  Such
thyroiditis is by far the most common reason for thyroid hormone

   You say:

   >>If T3/T4 levels depend upon sufficient dietary iodine to
allow the thyroid to respond to normal TSH levels, and the iodine
is missing or inadequate, TSH levels will rise as the body
attempts to boost T3/T4, creating the exact diagnostic picture
upon which synthroid is "indicated."<<

   Except for the thyroid enlargement.  People who are
chronically iodine deficient from dietary causes get goiters long
before they become more than marginally hypothyroid.  Possibly
they failed to tell you that in chiropractic school, since seem
to believe otherwise.  However, you are quite wrong if so.  To be
sure, not everyone getting 20 mcg a day of iodine or less
(typical for endemic goiter areas) gets goiter, and not everyone
with a goiter is iodine deficient (in certain coastal of Japan
where they eat lots of seaweed, the most common cause of goiter
is actually dietary iodine EXCESS).  But every person who is
significantly hypothyroid on the basis of chronic dietary iodine
deficiency, rather than intrinsic thyroid disease, will certainly
have thyroid enlargement by the time the hypothyroidism occurs.
This, for the basic reason that it takes a much worse iodine
deficiency to cause significant hypothyroidism than it does to
cause goiter.  Iodine-deficiency hypothyroidism is at the extreme
end of severity in endemic goiter, not the other way around.  If
you don't learn anything else from this message, learn that.  You
want us to believe that hypothyroidism from iodine deficiency is
common in North America, whereas goiter is obviously not (any
longer).  But anybody who knows anything about the thyroid will
know how wrong such a notion is.

   Iodine deficiency, whether you want to believe it or not, is
almost non-existent in our culture of iodized salt, and
interstate and routine international produce shipment.  To become
hypothyroid from low iodine intake in modern America you'd have
to live in a low iodine soil area, eat only produce from that
area (no seafood), take no multivitamin-multimineral, buy no
iodized salt or any processed foods which contain iodized salt,
and hardly ever eat out.  How many people do you know who THAT
describes?  And of course, you'd develop goiter first.

   Iodine deficiency does not cause single thyroid nodules.  And
people who see an M.D. for a goiter (general thyroid enlargement,
not a solitary nodule) don't just get a prescription for thyroid
hormone (unless the doctor is incompetent).  Generally, at that
point they get referred to an endocrinologist, since the average
internist is not usually going to work up a fresh goiter without
any referral.  (Perhaps the local chiropractor would?)

    The endocrinologist faced with a new diffuse goiter is going
to get a radio-iodine thyroid scan.  Goitrous iodine deficient
people have very good thyroid radio-iodine uptakes on scan, and
that strongly suggests the diagnosis of iodine deficiency (which
can then be confirmed at leisure with a history and 24 hour
urinary iodide excretion test).  The trace amount of radio-iodine
given is not enough to be dangerous, or to interfere with a 24
hour urine test.  But the rarity of iodine deficiency in the US
today is not only underscored by the rarity of goiter, but also
demonstrated by the extreme rarity of diffusely high iodine
uptakes in scans of thyromegalic people with normal or elevated
TSH levels.  Such scans are done, to be sure, but the results are
other than you see in deficiency.  Most thyromegalic people with
diffusely elevated thyroid radio-iodine uptake have suppressed
TSH's and Graves disease (they are often also clinically
hyperthyroid, never hypothyroid).  In the U.S., the remaining
people with goiter and high TSH levels almost always have low
radio-iodine uptake, and thus have goiter for reasons other than
iodine deficiency.

  >>I have yet to see a new patient who has not had the thyroid
gland surgically removed who comes to me already on synthroid
without an iodine deficiency.<<

    If so, then you are "diagnosing" what you call "iodine
deficiency" with some bogus chiropractic test that has nothing to
do with real biology.  Ridiculous.  Just as an aside, let me
remind you of the embarrassing fact that a good fraction of the
iodine in thyroid hormone is recycled by the body as iodide when
the hormone is broken down, so every patient you are seeing on
Sythroid 100 mcg is automatically also getting the equivalent of
65 mcg of elemental iodine also.  Thus, such people cannot be
very iodine deficient if they've been on replacement thyroid
hormone for any length of time (since, again, this repletes the
body iodine pool when the thyroid is working).  So this stuff
about them all being "iodine deficient" is quite obviously all in
your head.  Again, even if they WERE somehow iodine deficient
before, they aren't by the time they've been treated with thyroid
for a time.  As I said, if you think they are, you're using a
bogus test.

   For a physician it's rather easy to differentiate patients who
have burned-out thyroiditis from patients who don't, and who were
put on Synthroid by mistake.  You simply take them off Synthroid
for a couple of weeks and see if their TSH rises.  You know they
aren't grossly iodine deficient, because (again) all thyroid
hormone supplements are also iodine supplements (albeit expensive

   >> And I have yet to see a medical doctor in my area
evaulate for this simple nutritional portion of the

    That's because it's not necessary without goiter.  With
goiter, the iodine scan IS an adequate nutritional evaluation.
Which, if you knew anything about medicine, you'd have realized.

   >>Finally, I wish the issue of doctors ignoring their
responsibility to serve as teachers to their patients were purely
semantic, or that you understood the significance of words.<<

    Gee, I'm here teaching you about basic medicine for free,
aren't I?   How about the significance of actions?


From: B. Harris)
Subject: Re: Goiter
Date: 18 May 1997
Newsgroups: (Noel A. Taylor) wrote:

>>In the absence of other problems, such as tumors in the thyroid gland
>>>(usually palpated as non-tender and fixed) iodine supplementation is
>>>recommended.  Goiter is most commonly iodine deficiency, and used to
>>be quiteprevalent in the Great Lakes region (before iodized salt) due
>>to the virtual absence of iodine from the soils - and therefore the
>>foods - of that region.

   Comment:  But now that we have iodized salt, it is extremely rare
for iodine deficiency to the be the cause of a goiter in North America.
Noel is going you B.S.

    If you really want to know if a goiter is caused by lack of iodine,
you can get a first clue by looking at the ratio of T3 to T4.  In
iodine deficiency, the body adapts by converting from T4 synthesis to
T3, and the ratio of T3 to T4 in the blood (where T3 is expressed in ng
and T4 in mcg) climbs from a normal of around 15, up to an average of
30.  People with goiters from iodine deficiency are usually clinically
euthyroid, and have normal body temperatures and work capacities (ie,
they adapt well to the low iodine).  They sometimes (not always) have
mildly elevated TSH levels (making them subclinically hypothyroid by
definition), but these are (again) generally not in the range of people
who are clinically hypothyroid (the word "clinical" means "at the
bedside" and refers in this case to people with signs and symptoms of
hypothyroidism, not just an abnormal lab test).  People who are
clinically hypothyroid generally have TSH levels at least 4 or 5 times

   How people with iodine deficienct goiter can have normal TSH levels
(as they sometimes do) is a bit of a mystery, but evidentally has
something to do with conmpensatory mechanisms.  There is even evidence
that a hypertrophied gland becomes more sensitive to TSH.  Presumably
TSH needs to a elevated at least somewhat, for some period of time, for
the iodine deficient goiter to grow.  However, that can (though it does
not always) normalize later.

   A better test for iodine deficient goiter is a radio-iodine uptake
scan, as discussed in a previous message.  This is usually higher than
normal in iodine deficiency, although very occasionally even this falls
in "normal" range (normals here of course very with country to country,
depending on average iodine intake.  In the US, due to iodized salt,
normal iodine uptake is fairly low-- around 20-30%).  Very occasionally
an iodine deficient goiter will fail to concentrate iodine better than
average, for reasons that aren't too clear, but this also is rare.

   The gold standard for iodine deficiency is a 24 hour urine iodine
collection.  In countries where goiter is common, around 20 mcg per 24
hours is excreted.  Anything more than about 50 mcg means that the
goiter is almost certainly NOT related to iodine deficiency.  In the
US, average excretions are well above 100 mcg.

                                   Steve Harris, M.D.

From: B. Harris)
Subject: Re: Iodine Deficiency in N. America
Date: 22 May 1997
Newsgroups: (Ron Roth)
Subject: Re: Iodine Deficiency in N. America
Date: 21 May 1997 00:49:59 -0400
in Message-ID: <5ltutn$>

  >> I've encountered several thyroid specialists who certainly
wouldn't share that notion and consider standard blood tests only
marginally accurate to evaluate thyroid functions/disease.  In
fact, they have to put patients frequently on trial runs of drugs
when - in their  own words - "their symptoms don't coincide with
the blood tests." <<

   I've been known to do that myself occasionally-- however it's
very hard to support this with hard evidence that a deficiency in
the usual sense is being treated.  People with TSH levels in the
normal range invariably have no tangible or measurable signs of
hypothyroidism-- they have normal oxygen uptakes and heart rates
and body temperatures for age.  And normal DTR relaxation and all
the rest.  Some of them may not FEEL well in terms of energy, and
may feel better when given more thyroid, but it's more than a
little questionable whether thyroid hormone is here being used as
replacement or pharmaceutical.  Headache, after all, is not an
aspirin deficiency.  More to the point, you can treat obesity
with thyroid too, after all, but that doesn't mean that obesity
in all such cases is therefore due to hypothyroidism, either, or
that treating it with thyroid is necessarily a good idea.
Similarly, not all depressed or asthenic people who respond to T3
necessarily do so because they are "hypothyroid" in the usual
sense.  Some of them simply need a sympathomimetic kick in the
brain, so to speak, and would respond just as well to Ritalin or
Effexor or an MAO inhibitor.  Their brain catecholamine receptors
are down, but not necessarily because of low thyroid levels.

   >> You're telling Noel that an iodine deficiency is very rare
in North America.  Is that entirely based on those (theoretical)
reasons you  mentioned above, or have you actually tested
patient's iodine levels on a regular or long-term basis, for you
to reach those conclusions?<<

   There are lots of studies of average iodine excretions in
populations in North America, and they all average over 100
mcg/24 hours, with very rare to go below 50.  As I said in
another message.  Populations with a lot of goiter typically are
around 20.   Such data are used to decide whether or not to
increase iodination of salt or (in some countries) flour (there
are other uses for iodates in flour which have nothing to do with

   >> Does an assumed abundance of a chemical in the diet (as you
think of iodine) guarantee that everyone will enjoy "normal"
levels, and do you really believe that every case of iodine
deficiency will result in a goiter?<<

   Of course not.  What I said was that a case of chronic iodine
deficiency severe enough to result in clinical hypothyroidism
will be expected to result in a goiter first.  Most people with
goiters as a result of iodine deficiency are actually clinically
euthyroid, and haven't gotten to the clinically hypothyroid
stage.  On lab tests they are only marginally hypothyroid (ie,
subclinically hypothyroid, with slightly elevated TSH, low-
normal T4, normal T3, and elevated T3/T4 ratio)

   >>If you do, are you talking minimum goiter-preventative
amounts, RDA, or do you not consider that there is such a thing
as an OPTIMAL level of iodine?<<

    The RDA is chosen to be quite a lot more than the amount
usually associated with goiter.  Endemic goiter is very rare in
populations getting more than 50 mcgs per day.  There probably is
an optimal level of iodine which results in maximal goiter
prevention (somewhere around 100 mcg per day), but that is not
what Noel and I were discussing.  That conversation turned around
the question of the existence of non-goitrous subclinically
hypothyroid people in North America who were that way because of
iodine deficiency.  These, I said, are very rare.  How rare?
Like: show me one.

  >>Since your tests aren't able to establish optimal levels for
a patient and you therefore have to rely on AVERAGES and RANGES,
how do you know whether a goiter develops BEFORE
hypothyroidism? <<

   If you mean clinical hypothyroidism, I know because in
populations with goiters due to low iodine, most people haven't
yet gotten to clinical hypothyroidism, as noted.  As for
subclinical hypothyroidism due to lack of iodine, I suppose it
precedes goiter by a little while (the time it takes goiter to
grow), but you're not going to find one condition in a population
without the other, for obvious reasons.  Iodine deficient goiter
has been wiped out in the US, as shown by the normal T3/T4 ratio
and normal uptakes of the average euthyroid goitrous individual
in the US.  Thus, by extension, the same is true for
hypothyroidism due to iodine deficiency.

   >> - Do you really believe  that 'hypo' starts one decimal
point below 'normal,' where 'normal' can  be at the bottom or top
of your range - or at what point do symptoms  come into play for
diagnosis?  Do you think a patient's "normal" could  actually be
outside of your reference range? <<

    You can play that game, but it's awfully hard to prove.  How
do I know, for example, that the person who comes to me
with a normal body temperature hasn't got TWO strange things
wrong with them: 1) an abnormally low "normal" body set point (if
that isn't a contradiction), and 2) a chronic fever.  And the
answer is that I don't.  But I'm a fan of Occam's razor, and I'm
quite aware that you can too easily make a complicated hypothesis
to give any neurotic person a physical "disease" that way.  Just
hypothesize that "normal" for them is abnormal for other people,
and then hypothesize that THEREFORE their presently "normal" lab
values are really "abnormal" for THEM.  Voila!  Disease.

   The problem is: what do we say about diseases which we can
"make up" or imagine at will this way, and which there are no
tests for?  Are they "real," or do they exist only in our

   >> Now I could list a large number of cases, where my tests
indicate a typical thyroid deficiency in patients (while blood
tests are normal), and after my treatments (which often include
iodine), these patients feel better, their symptoms disappear,
and their thyroids test normal. But I know, in the typical
fashion of "medical science," this is termed a placebo, so I
humbly retreat and won't mention it again.<<


   >> OTOH, regarding your "low iodine doesn't cause hypothyroid"
claim...  YOUR PEERS "diagnose" hypothyroid, and prescribe
thyroid medication. <<

   They do, but not for iodine deficiency, where goiter will be
the presenting feature.  Again, low iodine does not cause
hypothyroidism in populations without some cases of associated
goiter.  My PEERS don't just willy nilly prescribe thyroid
medication for goiter, without tests which would also diagnose
iodine deficiency.

   >> I run a test and find both, low thyroid, and low iodine.
Patients  decide to take iodine only (no other medications), and
subsequent thyroid tests taken BY YOUR PEERS show all of a sudden
"normal" thyroid functions.  How is that possible?  Did the
iodine throw off your test, or is YOUR test suffering a placebo
effect now?<<

   I believe I'd like to see an example.

   >> Now, how about cases where there is a difference of opinion
the other way around --- where according to conventional tests
your peers believe that there is a thyroid deficiency.  However
my own test shows thyroid functions to be perfectly normal.
Perhaps in such a situation it is a bit more difficult for you to
claim a placebo effect.  While not as common, I come across this
scenario on occasion as well.  Here are the numbers for a
particular female patient:

 Total Thyroxine (T4)            56              60 - 155
 T Uptake                        0.34            0.22 - 0.34
 Free Thyroxine Index            19              13 - 53
 Thyrotropin (sensitive TSH)     14.63           0.35 - 5.00
 Antithyroid Microsomal AB       >2000           up to 20
 Antithyroglobulin Antibody      1025            up to 300

Since your numbers for T4 are "funny," by U.S. standards, I
assume you're using SI units of nanomoles/l.  Okay, I suppose
that Canada would do this (we've stayed with metric mcg/dl too
long in the US, but we'll switch soon also to SI).  This person
is hypothyroid by lab tests, and from the tests showing damage,
probably has Hashimoto's thyroiditis (especially if she has no
palpable thyroid on exam).  Certainly her problem is not iodine
deficiency (as you, I'm sure, know).  If she's not hypothyroid on
exam, that simply means she's only subclinically hypothyroid,
which is entirely possible.  Not everybody who falls below normal
lab range on T4 (especially if just barely) will have symptoms.
But if they have this much thyroid destruction, the process
generally continues, and they generally do become more even more
hypothyroid by lab numbers, and (of course) also eventually

   >>Ok, this patient has her annual physical and phones me with
the news that she's been found hypothyroid.  I look up her chart,
and it shows consistently normal iodine and thyroid functions for
the last several years.  So she asks me to run another test,
which turns out perfectly normal again.  I ask her if she has
_any_ hypothyroid symptoms at all - even very minor ones?  NOPE.
Ok, three weeks later she gets another thyroid test with convent-
ional medicine.  The numbers get worse:

 Total T4                         52               60 - 155
 T Uptake                         0.33             0.22 - 0.34
 FTI                              17               13 - 53
 TSH                              28.84            0.35 - 5.00

Her Dr is frantic by now and paints a very grave picture of what
will happen to her if she doesn't start on thyroid medication

   Well, if he does that, he's wrong.  Since she feels fine, it
obviously won't happen "immediately."  But it probably will
happen, and she should go on replacement, since she'll likely
need it soon (months to years), or else begin to suffer symptoms.

   >> Since I've come across this sort of thing with patients
from the US as  well, one can likely rule out any major
differences in the way US or Canadian Drs evaluate their
patients.   And for the record, I'm not telling her to disregard
her Dr's advice!
   So Steve, in your opinion, based on your infallible and
predictable medical science, what will happen to that patient,
and how soon, - IF  she decides not to follow her Dr's recomme-
ndations?  When will those hypothyroid symptoms finally kick in?
And if she continues NOT to take the medication, and nothing
happens...what's the medical term for that? <<

    I don't have the stats, but can tell you that most cases of
Hashimoto's go on eventually to clinical hypothyroidism once TSH
has significantly elevated, and the time-frame is months to a few
years.  Do I know that every last one does?  No.  It's possible
that this woman could go the rest of her life with what is left
of her thyroid pooping along making almost enough hormone, driven
by a pituitary working all the time like mad to flog it (ie, what
is happening above).   But it seems a silly thing to allow the
body to do.

   For one thing, if you don't give thyroid to this woman, you're
going to have to follow her with vital signs taken every 1-2
months to make sure she doesn't slip into clinical hypothyroidism
(or if she does, that you catch it early).  She has to be
compliant, and you have to watch her like a hawk forever.
Medically this is within the bounds of reasonableness (especially
for people who really hate pills), but it's a strain on everyone.
Doctors used to do this, BTW, in the bad old days when thyroid
blood tests were more expensive and there was no TSH test.
These days, it's a lot easier to get the subclinically
hypothyroid (high TSH clinically euthyroid) patient on a cheap
reliable replacement dose of thyroid, so you can forget about
when the crash is going to happen (checking her every year only,
once you get this adjusted).

   There are no bad effects from long term thyroid replacement,
so long as the dose is correct.  I believe you had claimed some
time ago that long term replacement causes problem with the gland
atrophying.  Not so.  The thyroid recovers within 1-2 months of
stopping long term replacement therapy, if it is going to recover
at all (ie, hasn't been destroyed by disease).  You once asked
for reference studies showing this, and today I happen to have
them at hand: N. Engl J. Med. 293: 681-84, 1975, and J. Clin.
Endo. Metab. 41:70-80, 1975.

                              Steven B. Harris, M.D.

From: B. Harris)
Subject: Re: Could be secondary hypothyroidism?
Date: 12 Feb 1999 08:03:13 GMT

In <> Nancy Parsons
<> writes:

>Hello -
>After several years of hypothyroid symptoms, but normal range TSH,
>a new doctor started a trial of Armour thyroid on the basis of

   If it was on the basis of symptoms only, with no prior testing, the
doctor is not being too wise.  The symptoms are nonspecific, and the
treatment is not without danger.  If the TSH and T4 were in the normal
range when treatment started, that automatically rules out secondary
hypothyroidism (pituitary failure) right there.

>After 8 weeks of supplementation with 1 gr., she ordered a TSH and
>total T4.

   For what reason?  If she's going to go by symptoms, she may as well
stick to her guns, don't you think?  <g>?   NOW she gets worried.

>The TSH came back in the normal range, 1.6 of 0.4-4.3, but the T4 and
>T3 uptake were both slightly low, despite the supplementation.
>Are these tests indicitave of secondary hypothyroidism?

   No.  T3 uptake has nothing to do with T3 levels.  The low TSH can be
the result of the T3 in Armor descicated thyroid, allowing a normal TSH
but a slightly low T4.  In fact, in people with no thyroid, you can
suppress TSH and correct hypothyroidism with T3 (Cytomel)
supplementation alone, and have no T4 in the body at all.  T4 is just a
prohormone, remember.  It doesn't do anything T3 doesn't.

>  And is any
>further pituitary testing necessary?

   No.  It's possible that a change in doctors may be in order, though.

From: B. Harris)
Subject: Re: Could be secondary hypothyroidism?
Date: 17 Feb 1999 04:21:52 GMT

In <> Nancy Parsons
<> writes:

>Going to trim the proliferation of attributions here....
>> > >Serum protein/albumin, etc.  As far as the thyroid, a physical exam
>> > >for enlargement, cysts, etc.  Perhaps an ultrasound, perhaps a
>> > >biopsy. But from the sounds of things, you could increase your
>> > >thyroxine dose.  How's your iodine intake, by the way?  (That's
>> > >necessary for thyroid function.)
>My iodine intake, as far as I can tell, is not deficient.  I take a
>multivitamin that supplements 150mcg, use iodized salt, and eat a
>reasonable quantity of seafood and locally raised (within 200 miles of
>the Pacific) produce.
>> How would you explain a normal TSH and a low T4, despite thyroid
>> replacement?  Could be any number of things.
>I'm confused as well.  One would expect low T4 to be accompanied by
>either a high TSH, or a low one, but not a dead-center normal one.

    Once again, for those of your who missed it, TSH is affected by T3
also, which wasn't ever measured, and which is being given also.  So
this patient didn't measure the T4 with the first TSH, and didn't
measure the T3 with the second TSH.  Without doing all three at one
time, there's no mystery to explain.

    If you simply MUST rule out hypopituitarism, there's always a TRH
test.  Any endo guy can do one, and they are simple and fairly cheap
office tests.  Get a shot, sit around a bit, get some blood drawn.
That's it.

From: B. Harris)
Subject: Re: Could be secondary hypothyroidism?
Date: 17 Feb 1999 23:18:27 GMT

In <> (Steve Emerson)

>Steven B. Harris ( wrote:
>:    If it was dangerous, it wouldn't have been taught in med schools.
>: I'll have to remember that argument.
>Either Barnes caused heart attacks during his years or
>he didn't.

   Sure enough.  Kindly point me to the published paper in which he
keeps track of his treatment group and shows that they have no more
cardiomyopathy or osteoporosis than expected.  Since of course any
group of patients will have SOME, just as a baseline.  I'd like to see
his P values.

> My own doctor has been using Barnes' approach
>for 30 years.  The AMA/state boards doesn't look kindly on even
>a single heart attack.

    The state boards have no way of knowing if a heart attack or a case
of heart failure or hip fracture was caused by inappropriate use of
thyroid medication unless somebody suspects and complains.  The coroner
certainly has no way to tell, even if an autopsy is done, which they
usually are not in non violent deaths, or deaths from degenerative

    A give me a break: EVERY doctor's practice has patients who have
heart attacks.  You have to die of something.  In my own geriatric
practice consisting of Mormon nonsmokers (mostly) who I have on vitamin
E and aspirin (when I can), homocysteine control, blood pressure
control, cholesterol control-- the whole bit-- I still ocassionally see
an MI.  All you do is cut the odds.  You never cut them to zero.

> My doctor wouldn't be in business if heart attacks were a result.

   Maybe he would and maybe he wouldn't.  Mild hyperthyroidism is like
smoking.  It destroys your heart and bones over decades, and sometimes
quite subtly.  And not in everyone.  You have to look at the animal
data (better controlled) or watch very closely in large groups of
people to see the effects.  But they are there.  You cannot just willy
nilly give everybody thryoid until their temperature comes up to 98.6.
If you'd like to give me your doctor's name, I'll be glad to let the
State Board know that's how he's doing it.  Then perhaps they will look
at the death certificates he signs a little more closely.  And if
you're going to tell me he never signs any death certificates because
his patient population is immortal, don't bother.

>I suspect that this heart attack
>scare is anecdote blown out of proportion by a profession which
>wants Dx procedures neat and convenient.

   Which wants them objective, where possible.  Giving thyroid to
everybody who feels cold is like giving testosterone to any man who
feels puny, or amphetamines to anyone with low energy.  Or, for that
matter, estrogen to any woman with hot flashes (no matter her other
risks and history of clotting). It's not good medicine.

> We can stop Rxing
>everything else which has Risk > 0%, aspirin for instance.

   Well, now you depart into a different area, which is philosophical.
Here, thyroid is being used essentially as a drug, not a hormone
replacement, because more is being given than the body wants to have or
make.  It's a bit like giving 3 grams of nicotinic acid a day for
cholesterol-- that's not nutritional or vitamin therapy, that's drug
therapy.   I don't really have a problem with that kind of medicine, so
long as everybody agrees that it's what's happening, and a drug which
may cause chronic problems down the line is being used to treat
symptoms NOW.  Quality of life for quantity of life tradeoffs are made
all the time in medicine, and it's okay so long as all parties are
informed.  Nobody thinks aspirin is risk free, but you apparently think
that giving people thyroid by titrating to body temperature, is.  And
that's probably what your doctor tells you.  Well, no ethical
transaction can be based on misinformation.

>:     Not that it was taught in my own med school, or that of any
>other doctor I've ever met.  But I suppose there's always the

>There was a time when low body temp with hypothyroid
>symptoms was enough to Rx thyroid.  If you want to make
>a wager with me, I bet I can find a medical textbook
>which argues that symptoms alone are sufficient to
>Dx hypothyroidism.

    No doubt one printed before there was a good way of measuring
thryoid in the blood (which used to be done by crude methods of
measuring total blood protein bound iodine, etc, before modern
radioassay changed all that.

   If you want to go back far enough, you can find medical texts that
say the darnedest things.   Masturbation used to be a disease, and
supposedly caused all kinds of physical problems.  It was put on death
certificates as a primary cause of death.  If you want some funny stuff
from old medical texts, I have lots.  But it is of mainly historical
interest.  One does not use it to justify clinical decision making in

>If you can point me to research which shows hearts attacks
>in people with normal heart and low body temp, cold
>extremities, fatigue, etc., I would be interested.
>This is one area of medicine in which progess has not

    I'll look, but I suspect that the doctors who treat such people
with large doses of thryoid don't keep careful records.  And the docs
who keep careful records wouldn't be so foolish.

                                       Steve Harris, M.D.

From: B. Harris)
Subject: Re: Could be secondary hypothyroidism?
Date: 17 Feb 1999 23:39:05 GMT

In <pTDy2.104$> "Nancy Wolfe"
<> writes:
>>From: B. Harris)
>In article <7adg50$>,
> B. Harris) wrote:
>>    Once again, for those of your who missed it, TSH is affected by T3
>>also, which wasn't ever measured, and which is being given also.  So
>>this patient didn't measure the T4 with the first TSH, and didn't
>>measure the T3 with the second TSH.  Without doing all three at one
>>time, there's no mystery to explain.
>Thank you for repeating this, I didn't see it the first time around.
>So, the next order of business is to get a complete thyroid panel,
>TSH, T4, and T3 simultaneously, yes?

   Correct!  And it must be done 24 hours after your previous thryoid
dose, not on a day of the morning you took one.  Taking levels on a day
you took thyroid (a common mistake) will give you  falsely high T4 and
T3 levels (if you're taking thryoid gland extract as you are, or some
other commercial fixed combo of these).

>>    If you simply MUST rule out hypopituitarism, there's always a TRH
>>test.  Any endo guy can do one, and they are simple and fairly cheap
>>office tests.  Get a shot, sit around a bit, get some blood drawn.
>>That's it.
>I've heard that this is a pretty difficult test to get ordered, and
>seeing as I'm probably paying for these tests myself, I think the thyroid
>panel first and then the other.  If there's indication, I would like to
>rule out hypopituitarism if I can; the thought of a slow growing
>non-secreting adenoma left undiagnosed is a bit distressing.
>Thanks for your help,

    Yes, I can see that, and agree on your plan.  As has been
mentioned, you can also look for panhypopit with an AM cortisol, or a
24 hour cortisol collection (cheap), or an FSH done in midcycle.  Or,
if you are postmenopausal or lacking ovaries, at any time.

From: B. Harris)
Subject: Re: Could be secondary hypothyroidism?
Date: 17 Feb 1999 23:50:24 GMT

In <7af644$i9j$>

>>     If you simply MUST rule out hypopituitarism, there's always a
>>TRH test.  Any endo guy can do one, and they are simple and fairly cheap
>>office tests.  Get a shot, sit around a bit, get some blood drawn.
>>That's it.
>Hypopit would not really seem to be a problem.	TSH comes from the
>pituitary, and it is normal.

    Yes, but perhaps (we're not sure) not normal for the amount of T4
and T3 in the patient's blood.  There's a suggestion not, since the T4
was low.  So we have to measure all three.   There are two questions
here: one of secondary hypothyroidism (TSH part of the pituitary has
quit doing a proper job) and one of panhypopituitarism (more than one
of the pituitary hormones function centers is not doing the job).  FYI
you can have one without the other, as tumors and other problems not
infrequently knock out pituitary fuctions one-by-one as they progress.
And as a rule it's the ability to respond to a stress with larger
secretion (a high TSH in reponse to lower T4/T3 or a TRH shot) that is
lost before complete ability to secrete is lost.   All of this is rare,
but if the T4 and T3 really are low, even if the TSH is in the normal
range, a stress test is probably warrented.  Nearly everybody with
secondary hypopituitarism goes through that stage on the way to losing
TSH completely, you know.  Which is to say, that for every person there
is a level of TSH between their normal level and the lower end of the
test boundary, which will result in them being subclinically
hypothyroid on the basis of free T4 and T3 levels.  Secondary
hypothyroidism is actually quite rare in medicine, but if you DO have
it, the picture we're seeing here is NOT rare as part of it.

From: B. Harris)
Subject: Re: Could be secondary hypothyroidism?
Date: 18 Feb 1999 00:07:38 GMT

In <7af644$i9j$>
>>and it is normal.

> The questions are: 1.  Why doesn't a normal TSH stimulate
>normal T4 and T3?  (cf. prior to treatment phase.)

    A good question, but we don't know if the T4 was normal prior to
treatment, unless I missed the post.  All that was gotten was the TSH.
The T4 may well have been normal at that time, and simply suppressed
later by the T3 in the thryoid extract.

>That could be medications or other things in the blood that would bind
>TSH and make it ineffective. (Haven't heard of this happening.) Could be
>that TSH is degraded faster than is normal.  (Haven't seen this diagnosed

   Yep.  Zebras.

>Could even be that the prior testing was inaccurate.  It would seem
>reasonable to boost the dose and retest all three components before going
>on a culprite investigation.

    Even more reasonable to stop the medication entirely, and do a
proper workup (this time) of the person in the natural state in a
couple of months. Because messes like this are what happen when you
don't do that to begin with.  Something I've been trying to explain to
the alternative types here, and not succeeding, dispite this nice
*illustration* case.  Remember that word?

                                     Steve Harris, M.D.

From: B. Harris)
Subject: Re: Could be secondary hypothyroidism?
Date: 18 Feb 1999 05:20:05 GMT

In <> (Steve Emerson)

>Steven B. Harris ( wrote:
>>    Which wants them objective, where possible.  Giving thyroid to
>> everybody who feels cold is like giving testosterone to any man who
>> feels puny, or amphetamines to anyone with low energy.  Or, for that
>> matter, estrogen to any woman with hot flashes (no matter her other
>> risks and history of clotting). It's not good medicine.
>Frankly, I think you folks have created a make-believe world.
>You don't think a person can tell when they are overstimulated?
>I don't buy it.  Insomnia, agitation, these things will be
>become apparent.

   Comment: So?  And the person will give up a drug which makes them
feel great and full of energy-- without having to do any hard exercise
every day-- just because of a little insomnia and agitation?

    A couple of million cocaine and crystal meth addicts in this
country say YOU'RE living in a make-believe world.  I KNOW what people
will do.  What alternative universe are YOU posting from?

> You docs are sending patients out of your offices
>who have cold extremities, fatigue, hypersomnia, and low
>basal temp with no thryoid Rx due, IMO, to unreliable thyroid tests,
>and you're justifying this as saving people from heart trouble??

    I'm sending a lot of wimpy guys out who claim our testosterone
blood tests are unreliable, and they really need to come up to normal,
in order to look like Arnold Schwartzenegger.

     Look, I must warn you that I'm a libertarian.  If it was up to me,
I'd give them the damn testosterone, so long as they knew the dangers
(which aren't, BTW, really horrible).   Adults ought to be able to take
risks.  I just object when people lie to each other about them.

>Unreliable thryoid tests have been the history in this area,
>and hypothyroidism as you know increases risk of cardiovascular
>disease, cancer, etc.  In fact as I understand, artherosclerosis can
>develop "rapidly", according to the medical text I just read.

   The medical texts are talking about people identified with those
thryoid tests which you claim are unreliable.  Can't have it both ways.
You find me the paper that says that atherosclerosis is a horrible
plague in people who have low temperatures as measured by a thermometer
stuck in their armpits (instead of under their tongues or looking at
their tympanic radiation), and who have normal thyroid lab studies, and
I'll listen to you.   Meanwhile, I think you're out in space.

>You want objective measures in contexts when none are often
>available.  Why don't you present the reality to the
>patient and let the patient decide.

    Cause not enough people voted Libertarian in 96.  Instead they
elected Clinton/Gore, who'd like government to be your partner, and
also be in bed with you.  And, needless to say, in the doctor's office
with us, when you visit me.  It takes a village to raise a child, you
know, and at least two more villages and several safaris to decide what
chemicals you can buy lawfully without permission from the State.  Try
to be more social.  What do you think you are-- an island?

> She is the one
>who is going to suffer the cardiovascular disease
>if these thyroid tests are just as unreliable as the last.

    Alas.  That's the trouble with laws.   Lawmakers don't suffer much
if they're bad.  I figured that out in highschool.  Where did YOU miss

    BTW, I might not agree with you about your need for more thyroid.
But my refusal to provide it in no way should be regarded as a vote in
favor of the idea that you shouldn't be able to treat yourself.

>Instead of hiding the reality and the risks and uncertainty
>behind a make-believe world in which things are black-and-white,
>why not let the patient take part in risk-assemsment
>and these judgements, rather than playing God, and using
>scare-tactics like "You can have a heart attack by
>a thyroid trial"?

    My world isn't black and white.  In the world, things are, however,
quite often legal or illegal.  I'm already on record as saying that
adults should be allowed to take risks, so long as they sign the paper
saying they read the official government and medical position about
what the risks are, and chose to ignore it.  And that they can't sue.
But don't hold your breath about how long it will take to get to that
kind of a world.

    As for me, I wouldn't take thyroid even if I had cold hands.  And I
wouldn't be caught dead with a thermometer in my armpit.

> Bejesus, folks with normal metabolism
>and normal thyroid are more likely to have a heart attack
>from an _expresso_ than fatigued people with cold
>extremities and low basal temp titrating on thyroid.

    How would you know that?

>No, not titrating to body temperature, because actually in some
>patients body temperature will not rise to normal, rather
>titrate to the whole collection of symptoms.  As to whether
>more thyroid is being given than the body wants, we
>really don't know whether the amount is exactly what
>the body wants or not.  But your argument, as I understand,
>that titrating to an amount that resolves symptoms,
>is more likely more than the patient needs , is not
>very persuasive to my mind, and in my opinion it is
>just as much a risk to do nothing and let sublcinical
>hypothyroidism run its course.

    Well, it's not persuasive to my mind, and all those speed addicts
is the reason.  You're not that great a judge of the optimal state of
excitation for your body.  Which is why nature, more or less, does it
for you.  If people want to freak out, it's up to them, for all I care.
But if you claim you're doing great at it, I'm going to disagree with
you.  I do agree that a LOT more study of physiologic responses to
thryoid are needed, and other ways to tell what the optimal over all
dose of thyroid hormone, if such exists, is for a given person.  But
nature is cruel, and there may not BE a single optimal level.  We live
ina world of tradeoffs-- dark skin now, skin cancer later.  Warm hands
now, osteoporosis later.  Learn to ski, risk skiing into a tree.  It's
all a matter of philosophy.  What a dislike is people who think it's

>Yeah?  All these patients with hypothyroid symptoms
>with normal tests?  I talk to them, and I was one of them.  Hoarse
>voice etcetera for 10 years.  I had thyroid panels maybe three
>different times, and all normal.

   So?   The symptoms of hypothryoidism are so nonsepecific as to be
nearly worthless.  They look like a combination of aging, couch
potatoism, chronic fatigue sydrome (which we now know is actually
caused by fluoridation, aspartame, and genetically engineered Gulf War
mycoplasmas), depression, AADD, and several personality disorders.
Lots of them can be fixed with Ritalin, and sometimes are.  But that
does not mean they are due to a Ritalin deficiency in the blood.  When
you give somebody thryoid, you simple upregulate the same receptors
that are stimulated when you give them amphetamines.  Yeah, they feel
better.  So blinking what?  I'm glad for them, but it changes my view
of physiology not a whit.

   Some years ago, as you may know, high cholesterols were actually
threated with D-thyroxine, the enantiomer of the normal hormone which
has very little activity.  And it worked.  Alas, it did have a LITTLE
activity.  And when they figured out how much, in terms of the real
hormone, they found they could lower cholesterol just as much by giving
that much extra real hormone.  Which had side effects worse than the
disease. A lesson there.

                                         Steve Harris, M.D.
                                         Speed Doc to Presidents

From: B. Harris)
Subject: Re: Could be secondary hypothyroidism?
Date: 21 Feb 1999 13:17:55 GMT

In <7ahilr$l71$>
>>     A good question, but we don't know if the T4 was normal prior to
>> treatment, unless I missed the post.  All that was gotten was the TSH.
>> The T4 may well have been normal at that time, and simply suppressed
>> later by the T3 in the thryoid extract.
>She had symptoms of hypothyroidism which were relieved by thyroid extract.
>That would indicate that one of the two was low.

    Nope.  "Symptoms of hypothyroidism" are all very nonspecific, and
usually are NOT due to hypothyroidism (as defined by lab test.  If you
define hypothyroidism in terms of clinical syndrome only, then they
always are.  But then we're just dealing in tautology).  Relief of them
by replacement is not indicitive of anything, unless again you decide
you want to define it as being so.  My position is that even if there
were no such thing as the placebo effect, some subset of people with no
energy really are helped symptomatically by being made hyperthryoid.
Just as they are, by being given ritalin (there's not much difference
between stimulating a receptor, and giving a hormone that makes more of
the receptor).  Except the thyroid is more dangerous.

   The fact that aspirin cures your headache does not indicate that the
headache was due to an aspirin deficiency.

>> >Could even be that the prior testing was inaccurate.  It would seem
>> >reasonable to boost the dose and retest all three components before
>> >going on a culprite investigation.
>>     Even more reasonable to stop the medication entirely, and do a
>> proper workup (this time) of the person in the natural state in a
>> couple of months.
>Yikes!	I recommended that one time to an attending in a patient with DI, and
>I was roundly criticized for it.

    As you should have been.  Hypothyroidism is not DI.  DI is
complicated by the fact that by drinking enough water you can create
inability to concentrate your urine for some time, even if you were
normal to begin with.  And this has nothing to do with the pituitary.
And untreated DI is dangerous, whereas untreated hypothyroidism for a
couple of months is not.  Assuming that the person has secondary
hypothyroidism with a TSH of 2, they certainly can't have been VERY
hypothryroid.  Unless they had BOTH primary and SECONDARY
hypothyroidism, or secondary PLUS iodine deficiency, or some incredibly
unlikely combination of problems.  Once again, you're hearing hoofbeats
and suggesting a zebra hunt.  Hell, a Przhevalski's horse hunt.

>Less disruptive to Nancy would be to repeat the test once she is
>stabilized on thyroid extract and repeat the test again in a few months.
>The repeat test will show a diminished TSH if there is secondary

    Yes, and it will also show a diminished TSH if her pituitary thinks
she's getting too much thryoid extract.  It's easy to lower somebody's
TSH by giving them a little more thryoid than they usually make.  Their
levels of T4 and T3 need not go above the "normal" range-- they only
need to go up from what they were (and are normally for that person).
But these people have perfectly normal pituitaries, as shown by ability
to respond to a TRH test. The only way to argue that they have abnormal
pituitaries, is (once again) to *define* secondary hyopothryoidism as
that condition which results in TSH in the normal range, and T3 and T4
in the normal range, in a person who feels they *ought* to have
something different-- to wit: a higher T3 and T4, and a lower TSH.
This is scientific endocrinology however.    If you want to increase
your homone levels until you feel good, fine.  But please don't tell me
you have a disease or pathological condition, as a result.  Unless the
pathology is somewhere in your attitudes.

>> Because messes like this are what happen when you
>> don't do that to begin with.
>I don't think I'd want to criticize the care as a "mess", exactly. The
>treatment she was afforded did help her, and she has a few remaining
>symptoms which could be treated with a bit more extract.

   The treatments she was afforded helped her symptoms.  That may be
placebo effect or too much T3.  Either way, it's not the practice of
good medicine to decide you've got a disease.  And the side effects of
artificially increased T3 may catch up with her one day, feel good or

                                    Steve Harris, M.D.

From: B. Harris)
Subject: Re: Could be secondary hypothyroidism?
Date: 21 Feb 1999 13:39:17 GMT

In <4GYy2.88$> "Nancy Wolfe"
<> writes:

>Thank you so much for this clear and cogent explanation of what
>might be happening.  I had never considered the test results in
>the context of a potentially progressive process before. I was
>thinking of them as an indicator of state, sick/not sick, not as
>a point on a spectrum.  This is probably my CS bias showing :-)
>It looks like from what you're saying that normal values on the
>other pituitary hormones wouldn't necessarily rule out a pituitary
>problem, is that so?  If that's true, at what point do I start
>thinking of a CAT scan or an MRI to look at what's up there?

   When you get vision problems, headaches, visual field cuts on
testing, or when any of the pituitary stress tests I mentioned come out
abnormal.   Being in mid-cycle or postmenopausal is a sort of pituitary
stress test for FSH.  So is the TRH test, for TSH.  And there is a test
of ACTH secretion called the Cortrosyn stimulation test, which is
analogous for that function.  Again, an endocrinologist can help you
with any of them.

From: B. Harris)
Subject: Re: Could be secondary hypothyroidism?
Date: 22 Feb 1999 01:26:31 GMT

In <> (Mark London)

>In a previous article, B. Harris) wrote:
>>In <> (Steve Emerson)
>>writes: Whether it's
>>>nerve conduction studies to Dx nerve compression, MRI's
>>>to Dx MS, mercury blood/urine tests to Dx mercury
>>>poisoning, or thyroid tests to Dx hypothyroidism,
>>>you folks are busy constructing and promoting the
>>>illusion of perfect information.  Why?  Because
>>>it serves patients?  No, because it makes your jobs
>>    Nah, it just saves us from diagnosing anything we or the patient
>>feels like.  Which helps to prevent disease-of-the-month syndrome with
>>attendent cure-du-jour.  Of course, doing it the other way is actually a
>>lot easier.
>You are missing the point.  What you should be doing is paying attention
>to the patient's symptoms first, and only using lab tests as a tool. If
>all the labtests are negative for hypothyroidism or any other disease,
>yet the patient still has hypothyroidism symptoms, do you tell the
>patient to ignore the symptoms, or do you suggest trying some vitamins or
>minerals, or at the very least do you try a course of thyroid
>supplementation? I think that is the issue.
>Mark London

   I have actually given patients very small amounts of thryoid for
symptomatic reasons-- enough to suppress TSH into the lower ranges of
normal.  But I'm not sure I'm not doing long term harm, and I explain
this to patients (it's rather like treating arthritis pain with
antiinflammatories, when you're not sure you won't cause a fatal GI
bleed.)   Thyroid this way should not be thought of as a hormone
replacement, but rather a pharmaceutical.   You get NO points from
mother nature for using natural compounds in an unnatural way.   You
might as well use an MAO inhibitor, or an amphetamine.  Which, in a
very few cases, I've done also.  This is pure treatment of symptoms,
like giving long term narcotics for chronic artritic pain.  Usually,
it's a nasty tradeoff.  When it's done, all parties should understand
what they're getting into, and what risks they are really taking.  So
when the party of the first part has a broken hip or a stroke or an
addiction later, they don't blame their doctor for being a quack.

   My problem with your post is that it seems to lack as sense of
proportion and balance, and the suggestion that treatment of symptoms
without a diagnosis (which is not wrong per se) can come "free," if
only the treatment is a natural item.  This is dead wrong.

                                   Steve Harris, M.D.

From: B. Harris)
Subject: Re: thyroid question
Date: 9 Mar 1999 14:04:33 GMT

In <7c1old$t24$> "medgirl"
<> writes:

>I just got my results back from a thyroid test and had a low TSH (0.04)
>and high T4 (12.3). The thyroid hormone binding ratio was .77 (normal is
>.81-1.21) and my free thyroxine index was 9.5 (normal is 5.2-11.0). The
>binding ratio is inconsistent with hyperthyroid and suggests problems
>with TBG. All of my symptoms are hypothyroid, not hyper - cold
>intolerance, clinical depression, weight gain of 30 lb. in the past 1 1/2
>years.  Is it possible to be hyperthyroid and have all of the opposite
>symptoms?  Any ideas as to what this means?
>*remove nospam to reply

    You should of course have the tests all repeated before you do
anything.  Assuming they come out the same, a low TSH means you are
hyperthyroid, unless your pituitary is not working.  Which would mean
in your case that you had two problems at once (since your thyroid
gland is working great, to say the least).  Which is incredibly
unlikely (that you have two problems at once).  Odds are, instead, very
good that you have a thryoid nodule making too much hormone.  A
radioactive iodine scan will show it, if so.   But your endocrinologist
has already told you this, right?

    Your symptoms are nonspecific, and could be from many things.
There are also lots of reasons for an abnormally high amount of TBG,
even when hyperthyroid.  In any case, have the scan done, and take care
of the nodule if you have one.  Then see see about the rest of your

From: B. Harris)
Subject: Re: thyroid question
Date: 10 Mar 1999 11:32:06 GMT

In <> David Rind
<> writes:
>Steven B. Harris wrote:
>> In <7c1old$t24$> "medgirl"
>> <> writes:
>> >
>> >I just got my results back from a thyroid test and had a low TSH
>> >(0.04) and high T4 (12.3). The thyroid hormone binding ratio was .77
>> >(normal is .81-1.21) and my free thyroxine index was 9.5 (normal is
>> >5.2-11.0).
>> Odds are, instead, very
>> good that you have a thryoid nodule making too much hormone.  A
>> radioactive iodine scan will show it, if so.
>>     Your symptoms are nonspecific, and could be from many things.
>> There are also lots of reasons for an abnormally high amount of TBG,
>> even when hyperthyroid.
>I have to disagree with Dr. Harris about the nodule. I think
>he is applying a geriatric mindset to someone who I suspect
>is a bit younger (given the handle "medgirl").
>The most common cause of hyperthyroidism in a young woman is
>likely to be Graves' disease.  For an acute presentation,
>subacute thyroiditis is common, and Hashimoto's can cause
>hyperthyroidism early in the disorder.  Hyperthyroidism from
>hot nodules is less common in young people.

    Yes, though it's not rare even in young people.  But I agree-- in a
woman of 30 tru hyperthyroidism would be more likely Graves'.  The
problem is that none of the primary thyroid problems give you high
TBGs, obviously, so all of this is academic.  It doesn't fit either
scenario.  Perhaps I'm guilty of assuming that if she had Graves or one
of the acute thryoiditis syndromes (leaving out early Hashimotos, which
is often not tender or apparent), she would have noticed a funny
thyroid, and said something.  And at some age the nodule people surely
begin to outnumber the asymptomatic throat people who have
Hashitoxicosis.  What age would that be, I wonder?  Closer to youth
than old age even in the US, I would suspect.  But it will take a trip
to medline to see.

  If her neck is normal and she's not pregnant or taking BCPs or some
other odd drug, probably the next thing to do would be look at some
liver enzymes.  But how to explain the low TSH?  This is a mystery.

>A high TBG in a young woman is frequently due to oral

   Yep, or preganacy.  But in that case, again, TSH will be normal (I
think you can see low TSH in hyperemesis gravidarum, but I sure don't
remember a case from med school, and we saw a lot of hyperemesis).  And
if her TBG really is high, as here, that's as far as you have to look.
in the direction of the thyroid (if it's grossly normal).

> In medgirl's situation, the TSH is somewhat
>low, and the free thyroxine index is normal.  Usually, I'd
>plan to either get a thyroid scan or just repeat labs in
>a month or two in a situation like this.
>David Rind

    Yes, if the person is not tachycardic or hypertensive and you can't
feel a nodule, you can wait. Alternately, the scan will show you Graves
just as well, if you suspect it from exam.   The problem is this woman
doesn't fit any good picture.  If there's something wrong with her
thyroid, there's something ALSO wrong with her liver too (or she's on
some drug).   Time to repeat the tests!


From: B. Harris)
Subject: Re: thyroid question
Date: 10 Mar 1999 11:39:11 GMT

In <7c3suj$q8k$> "medgirl" <>

>Steven B. Harris wrote in message
>>    Your symptoms are nonspecific, and could be from many things.
>>There are also lots of reasons for an abnormally high amount of TBG,
>>even when hyperthyroid.  In any case, have the scan done, and take care
>>of the nodule if you have one.  Then see see about the rest of your
>Thanks for your advice.  I'm having a scan done in a couple of weeks and
>a blood test for the Hashimoto's and Grave's antibodies.  Hopefully that
>will straighten things out.  I don't relish the idea of taking thyroid
>suppressants and making my current problems worse.  Yes, they are
>nonspecific and may have nothing at all to do with the thyroid, but
>suppressing the thyroid doesn't seem like it would be helpful with the
>cold, weight gain, etc.
>It's a little frustrating as the only reason I had the TSH done in the
>first place was to see if there was an outside chance of thyroid problems
>contributing to my depression and now I have all this other stuff to deal
>with - if it hadn't been for thinking I was hypo, I never would have had
>the test done in the first place!
>*remove nospam to reply

   Yeah. Well, if you're not pregnant or on oral contraceptives, and
you can't feel your thyroid and it's not tender, it's worth repeating
the TSH before you go into all that expensive stuff.  It may just be a

From: B. Harris)
Subject: Re: thyroid question
Date: 11 Mar 1999 06:20:06 GMT

In <7c5mpc$aa0$> "medgirl" <>

>Steven B. Harris wrote in message <7c5lkv$>...
>>   Yeah. Well, if you're not pregnant or on oral contraceptives, and
>>you can't feel your thyroid and it's not tender, it's worth repeating
>>the TSH before you go into all that expensive stuff.  It may just be a
>They did it twice, about a week apart - first time .05 and second time
>04. My doctor said my thyroid felt enlarged on one side, although I can't

   Interesting.  Well, then, probably some kind of primary thyroiditis
(an infection, usually), and if your heart rate isn't too high, as Ed
says, you may be able to just watch for a while and see if it goes
away.  If not, a scan will tell you if you have Grave's disease vs
something else.  Treatment for this (Graves') is tricky in young
people, due to our limited follow up time for radioiodine ablation
(gland killing).  It's only out to 40 years, or something.  So for
someone who has more than that life expectancy, there's a fear you
might do more harm than good with that.  The remaining choices are drug
suppression or surgery.  The first has side effects for many and is
expensive.  The second is painful, has complication possibilities, and
has its own risks.  Hopefully you have the kind of thyroiditis that
resolves on its own (which even Graves' does, now and then).

                                     Steve Harris, M.D.

From: B. Harris)
Subject: Re: thyroid question
Date: 11 Mar 1999 06:26:01 GMT

In <7c5nht$d8o$> "medgirl" <>

>Steven B. Harris wrote in message <7c5l7m$>...
>>    Yes, if the person is not tachycardic or hypertensive and you can't
>>feel a nodule, you can wait. Alternately, the scan will show you Graves
>>just as well, if you suspect it from exam.  The problem is this woman
>>doesn't fit any good picture.  If there's something wrong with her
>>thyroid, there's something ALSO wrong with her liver too (or she's on
>>some drug).  Time to repeat the tests!
>I am 24 and I am taking oral contraceptives.  No family history of
>thyroid or autoimmune problems.  My liver enzymes (AST and ALT) were
>elevated, but just out of the high range of normal, not grossly elevated.
>I asked my doc if the birth control pills could be causing the abnormal
>lab values and she said it messes up the validity of the T4 as a
>measurement but doesn't explain the very low TSH.

   Correct!  So there we are.  Ed was right.  Your thyroid really is
the problem, and your birth control pills are just fouling up validity
of the T4 part.

    Most studies show that even asymptomatic people who are
hyperthyroid enough to have suppressed TSHs are at risk for
osteoporosis and some other problems.  So whatever you have, if it
doesn't go away in a few months, you'll have to do something about it.

>The only "symptom" I've noticed at all is that my resting pulse rate is
>higher than it used to be - about 80, wheras it used to be more like 55
>or 60.  I was wondering - could it be that I'm just at a really early
>stage of whatever is going on?  I didn't have the TSH checked because of
>hyper symptoms, but for totally different reasons.  Maybe it's just not
>clinically apparent yet?

   Most likely.  You're not tremendously hyperthyroid-- just barely.
If you really want to see how high your T4 is compared with normal you
can get a free T4 by equilibrium dialysis.  A test done often on
pregant women in whom there are problems.  But more than likely your
TSH is good enough, since your pituitary does that kind of thing, and
is almost certainly working fine.  Your present values are quite enough
to send you to a scan if they continue.


From: David Rind <>
Subject: Re: Of the subject just a second
Date: Mon, 22 Mar 1999 10:37:32 -0500

NanL wrote:
> Thank you Steven,
> It is the symptoms from the low T3 that I am
> curious about and where can I find the info on the
> hot debate?

If you want to look at primary literature, you can
take a look at the Feb. 11th, New England Journal, or
look online at:

I've been a major skeptic, here and elsewhere, about people
who claimed to feel that they were not adequately replaced
on levothyroxine that was sufficient to normalize the TSH.
The above study, though, really calls this into question,
and raises the possibility that some (or all) people on
thyroid hormone replacement should be given a mixture of
T3 and T4.

David Rind

From: David Rind <>
Subject: Re: Of the subject just a second
Date: Mon, 22 Mar 1999 17:46:00 -0500

Anna wrote:
> Hi David. Isn't there a lot sideeffects to T3 supplementation? I'm not
> sure but I think I have read this somewhere. Do you also know if it is
> the T4 that regulates TSH? Or if it is the more active T3, that would
> explain a lot in some strange cases I think  :))

It's not so much that there are side effects as that it is felt
to be less safe.  T3 is the major active form of the hormone, and
T4 acts mostly by being converted to T3.  If you give a bit too
much T4, the body downregulates the conversion to T3 which helps
protect against hyperthyroidism.  If you give too much T3, it
acts directly and rapidly, and so can potentially be dangerous.
The editorial (one of the two articles I posted the URL for
previously) argues that we should be using combination T4/T3 in
a ratio that is not currently commercially available, and that
the T3 should be in slow release form to be safe.

It had been felt that TSH responded appropriately to T3, but
the NEJM study suggests that T4 may, as you imply, be more active
on the pituitary relative to the rest of the brain/body.

David Rind

From: B. Harris)
Subject: Re: B-complex and iodine questions
Date: 13 Apr 1999 12:32:31 GMT

In <>
(Michael A. G. Cohn) writes:

>I'm trying to buy some supplements for my family, but I've run into a
>few problems. Can anyone advise me on:
>1) B vitamins:
>Most products seem to offer high (10-20X RDA), but otherwise random,
>levels of several B-complex vitamins. I understand that at this level
>these water-soluble vitamin are non-toxic and may be helpful. However,
>I do recall reading that the B vitamins are uptaken competatively, so
>that high levels of one may induce deficiency in others. Does anyone
>know if this is significantly true?

   No, it's one of the great myths of nutrition.

> If so, what are the proper ratios
>to shoot for, and what kind of range is appropriate? I'm especially
>concerned because none of the supplements I've seen contains B12.

    Take a couple of RDAs of the B vitamins and you'll be fine.

>2) Iodine:
>What is the toxic dose of iodine? Consuming as much salt as we do
>(including salt we add to recipes or sprinkle on ourselves, so I know
>that at least a good bit is iodized), I suspect we're never lacking in
>it to begin with. However, it is also nigh-impossible to find a
>mineral supplement that doesn't pile it on in half or whole-RDA doses.
>How much can one safely take?

   No good answer to that, since there are a few people who become
hyperthyroid if they get more than a fraction of the RDA of iodine.
That is, they have a problem with their thryoids which is held in check
by a marginal supply.  Supply the stuff to a population, and these
people always pop up (von Basdow's syndrome).  For everybody else,
large doses of iodine suppress thyroid function temporarily, but it
recovers.  Huge doses can be taken safely for years by those with
normal kidneys (thousands of times the needed RDA), and once were, as
expectorants.  Excess, which is water soluable, is simply urinated off

From: B. Harris)
Subject: Re: Thyroid TSH levels
Date: 18 Aug 2000 09:27:44 GMT

In <> Paul Burridge
<> writes:
>I'm still puzzled, however. I was under the impression that
>hyperthoyroidism was associated with intolerance of heat, whereas
>hypothoyroidism was associated with cold intolerance. I've developed
>an intolerance of heat but appear to have a reading that (at 11.2) is
>*supposed* to be cold intolerant. What's going on? I've read all the
>heavyweight text books on the subject but still can't figure it out
>(other than the fact that endocrinology is no simple matter, that is).
>Have I too much or too little of whatever it is I'm supposed to have,
>or not have, depending on how demented you are by the time you get to
>the bottom of all this crap?

  Don't worry about whether your symptoms are "right" or "wrong". I've
seen them all over the map, including new dysrhythmias in hypothyroid

  Get some thyroid hormone, and with your doc's monitoring, dose to get
your TSH below 5 and (ideally) down around 2.  Then see what your
symptoms are like. Remember not to take your pill on the day of blood
testing, until after the test is done.

From: "Steve Harris" <>
Subject: Re: Do Japanese develop hypothyroidism?
Date: Sat, 5 May 2001 17:25:53 -0600

> On a more general note there are claims that 10% of Americans have low
> thyroid function.  Is there any truth to this or is it a case of
> "don't you wish" reasoning to rationalize the high levels of obesity.

I don't know what the % is, but low thyroid function, if you define it by
rising TSH levels, is usually completely asymptomatic. It is farily common,
and often seen in women with Hashimoto's disease. Doctors generally start
considering thyroid supplementation at TSH levels above about 5, but this is
preventive, since such people usually keep right on going into symptomatic
territory as their thyroid disappears from autoimmune destruction. The
average symptomatic person has a TSH around 10, though.

As for obesity, almost never does it have anything to do with thryoid
function. Even people who are honestly hypothryoid rarely gain more than 10
or 20 lbs, and often don't gain anything.  The epidemic of obesity you see
in America is due to a capitalistically-driven convergence to a market of
pre-prepared high-fat calorically dense foods. Capitalism gives people what
they want, and alas, what we want is calorically dense foods. We came from 2
million years of starvation-- what do you expect?  Technology drives all
this, of course. Fatty food tends to spoil, but Crisco doesn't, and we're
getting much better at packaging and preserving the rest. Freezer to
microwave culture has nailed us, as has fast-food in all forms.

You can give somebody enough thryoid to make them lose weight, but that's
using thyroid rather as a semi-sympathomimetic stimulant (thyroid makes
sympathetic functions work better).  The old give-em-speed avenue for fixing
everything (including your weight) is a major trick of the speed-doc crowd
that pushes stimulants for whatever ails you.  Dexatrim, thyroid, Dexedrine,
Ritalin, phentermine, phenylpropanolamine, ephedra, Welbutrin, cocaine-- we
like all this stuff. The shrink term for it is "activating."  As in: "I'm
going to prescribe you an activiating medication." Learn the lingo, and you
too can get a prescription to fly.

> What effects, if any, to weightloss would you attribute to
> supplementing with free tyrosine?

It's a precursor to sypathomimetic chemicals in the body, and acts as a mild
drug of this class.

> I have lost 22 kg and am wondering what else to do to lose say another
> 3 kg.   Would high tyrosine foods have any effect?

Have no idea.  The amino acid itself on an empty stomach is only mildly
activating <g>, so I'd be suprised if high tyrosine foods, with all those
other competing large neutral side-chain amino acids, would even do that


From: "Steve Harris" <>
Subject: Re: Raw Glandulars and the best selling pills
Date: Mon, 8 Apr 2002 18:10:14 -0600
Message-ID: <a8tbqh$9cj$>

<> wrote in message
> Hi,
> My DH is going to a nutritionalist who has prescribed thyroid
> glandular's from a bovine source.  Is there any scientific data behind
> this kind of treatment?  Does it acturally work?


It shouldn't, as by law all such products must have the active thyroid
hormone removed from them, and that hormone is the only thing that WILL work
(even though dangerous) for weight loss.

For some time I've had a sneaking suspicion that thryoid hormone is being
used in the US for many reasons other than to treat Hashimoto's disease and
similar low thyroid states. We know that shrinks tend to use it as a pep
pill, somewhat like the poor man's Ritalin. And it does induce weight loss.

The number one drug, by number of prescriptions written for it in the US in
1996 was Trimox (amoxicillin suspension), a cheap treatment for pediatric
earaches and general all around everything pediatric placebo.  #2 was
Premarin conjugated estrogens.  Well, lookie, the top two drugs are for the
main problems of a woman's life: screaming kids the first half, looking too
old to have them the after that. #4 is generic hydrocodone.  Cures all the
pains of life for both sexes. #5 is Zantac for that sour feeling you get
with the boss. #6 is Prozac. Enough said.

But #3 is Synthroid, the best-selling thyroid pill. Can genuine thyroid
problems *really* be that common? As common as these other things? I frankly
don't believe it; so call me skeptic.


From: "Steve Harris" <>
Subject: Re: Low Thyroid and Anemia?
Date: Sat, 20 Apr 2002 15:48:38 -0600
Message-ID: <a9snpt$r4t$>

"John Riggs" <> wrote in message
>     IMO, TSH, as a "Gold Standard" for defining hypothyroidism, is a farce.
> A better definition requires using TSH as a *flag* only to screen
> potential cases which should be better defined by T4 and T3 ( both bound
> and unbound ). If the actual thyroid hormones are lacking in
> sufficiency, there is a definite case for treatment, as TSH is a
> stimulating hormone only and has bearing upon the metabolism only as
> much as a gas gauge in your car tells you you need more gas. Knowing you
> need gas does not mean you have run out, only that you most likely are
> preparing to run out soon, and even then, the accuracy of the gauge is
> subjective and open to scrutiny, in fact, the gauge may be wholly
> erroneous. Only with further testing of the system can one be absolutely
> certain.


The problem with this analogy is that we know very well your car runs just
as well with the tank 1/4 full as it does when it's completely full. We
don't know that about the body, and for some biological systems its works
that way, and others it clearly doesn't.

Example: I put you on Everest basecamp. Assuming you have some low O2
sensors and your body is working okay, you'll begin to hyperventilate to
bring your CO2 down and O2 up (if your body can't do this, you get mountain

BUT your body never brings O2 back to quite where it was this way, because
if it did, the extra respiratory drive would be lost and then you wouldn't
hyperventilate any more. The same happens in spades as you continue up the
mountain over the next weeks.

It's the same if I add acid to your blood-- you'll hyperventilate to bring
your pH up-- but never completely to normal, or otherwise the drive would be
gone and your pH would go back down.

If you have a high TSH this means your pituitary cells are "hypothyroid"--
some of them aren't seeing as much T4 (and in the end, T3) as they'd like to
see. They're hurting, or else they wouldn't be screaming. The question is
whether or not this is true for other cells in your body as well. If I was
nature, I think I'd have designed the system to give the non-linear panic
signal (TSH here goes to 5 or 10 times normal) at JUST the point where
you're about to have problems-- like those gas needles that oscillate to get
your attention near empty. Slightly elevated TSH is a bit like hunger or the
feeling of HOT on your skin. Highly elevated TSH is more like the
oscillating low gas gauge or the feeling of pain with heat-- we know that
happens at exactly the temperature at which thermal skin damage begins.
Forget the gas gauge. I suspect that ignoring a TSH of 10 because T4 is
hasn't gone below normal is more like ignoring your dipstick because the oil
light isn't on.


From: "Steve Harris" <>
Subject: Re: Low Thyroid and Anemia?
Date: Sun, 21 Apr 2002 17:51:36 -0600
Message-ID: <a9vjik$b6j$>

"Simon Waters" <> wrote in message
> Steve Harris wrote:
> >
> > (though treating does raise people's anxiety levels-- surprise).
> Did I misread your post?
> It said it was a double blind trial, and anxiety rose
> significantly only in the thyroxine treated group, thus it is
> treating with thyroxine that makes people anxious, not treating
> in general.

I meant of course, treating their subclinical hypothyroidism.  With

Sigh. If you write something in a way that CAN be misunderstood, somebody
WILL misunderstand it.

From: "Steve Harris" <>
Subject: Re: Re Immune system and fish oil.
Date: Mon, 28 Apr 2003 11:06:38 -0700
Message-ID: <b8jqn9$mek$>

Tea Cup said:

> The Japanese also eat a lot of kelp, nori etc and that helps strengthen
> their thyroid which extends life.

 This is nonsense. If anything, the Japanese high
 iodine intake causes them thyroid suppression problems,
 which show up in the coastlines as a higher incidence of
 symptomatic marginal Hashimoto's disease (an autoimmune
 thyroid disease, but one in which marginal thyroid function
 is capable of being surprised with high iodine levels, when
 it is in trouble already). Iodine intakes above RDI do NOT
 stimulate the thyroid, but rather the opposite. That's one
 of the more pervasive myths of alternative medicine. People
 who know physiology know that iodide may even is used to
 treat thyroid storm.

 This isn't even getting to the question of whether a higher
 thyroid status would be life-span extending, if you could
 arrange for it (by, say, taking the hormone). I know of no
 evidence for it. Evidence in animals is all against it.


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