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From: B. Harris)
Subject: Re: Iodine is n't it toxic?
Date: 27 Dec 1997 20:07:22 GMT

In <6838qc$kua$>
(Marion Umowski) writes:

>As a child, I was given Iodine granules mixed in honey by my parents,
>and I can't imagine why. Was it ever believed to be beneficial?
>Obviously it didn't harm me, but I don't think it could have been good
>for me either.

   Well, the crystals are a pretty good water antibacterial for
polluted waters.  It's possible they might have some medicinal
(antibacterial) properties in the gut, but they aren't used that way
today because they are mildly caustic.  You might ask a pharmacist what
pharmacies carried elemental iodine crystals for.  And ask soon,
because they probably won't be for very much longer (they are a popular
starting material for the reactions used by illegal "meth" or
methamphetamine home-brew labs, and the authorities will probably do
something soon to control their availability to the general public.
All those kids making the touch sensitive explosive NI3 all those years
didn't get I2 off the shelves, but the drug trade probably will).

   I can't imagine what else I2 might be good for.  Iodine salts in
high concentations are expectorants, like guifenisin.  But that's a
different chemical state of iodine, and when you eat the pure element
as a solid you don't get much of the iodide salt.  Antibiotic iodine
tinctures, BTW, contain large amounts of both iodine and iodide, due to
the poor solubility of elemental I2, and the much better solubility of
the odd species I3-, which dissociates easily to I2 and I- and thus has
similar antibacterial properties to the element.

                                         Steve Harris, M.D.

From: B. Harris)
Subject: Re: Iodine is n't it toxic?
Date: 29 Dec 1997 10:34:47 GMT

In <687n9n$o2d$> Bryan Shelton
<> writes:

>Steven B. Harris <> wrote:
>: <<snip>>
>: All those kids making the tough sensitive explosive NI3 all those years
>: didn't get I2 off the shelves, but the drug trade probably will).
>Oh, man!!  Now you're bringing back fond memories from my childhood!
>I use to play with nitrogen tri-iodide all the time.  You could put
>a tiny bit of that stuff on a door-knob, let it dry, and the first
>person to walk through the door, BANG!  You could scare a person
>half to death with it.
>And we used to get old medicine capsules, empty them out, and fill
>them with dry tapioca with a little glob of nitrogen tri-iodide in
>the middle.  Then you wait exactly ONE DAY (any longer and they'd
>be too sensitive to handle).  Then you could (gently) carry them
>around;  throw one to the ground or at a friend, BANG!
>Ah, to be young again!

   If you coat tiny pieces of hamburger with it, you find that it's
capable of being set off literally by the touch of a fly.

    You're right.  In the world to come you won't let kids do such neat
stuff.  Or let them make the fine explosive silver acetylide out of old
coins, either.  Coins are long since made of something else.  <g>


From: B. Harris)
Newsgroups: soc.culture.indian,,soc.culture.indian.delhi,
Date: 28 Jul 2000 10:06:50 GMT

In <> (Dr. Jai Maharaj) writes:
>According to Dr Kapil, daily Iodine intake of upto one mg
>(1000 mcg) appears to be entirely safe.

   Again, it causes a certain number of Jod-Basdow syndrome
(hyperthyoidism due to iodine-stimulation of otherwise clinically quiet
thryoid nodules). When the Tasmanians added iodine to their bread, they
had a pretty good outbreak.  Nothing is free in public health.

From: "Steve Harris" <>
Subject: Re: Do Japanese develop hypothyroidism?
Date: Tue, 1 May 2001 18:12:21 -0700

John De Hoog wrote in message <>...
>"Steve Harris" <> wrote:
>> >To get back to Quentin's original question: maybe the Japanese don't
>> >avoid hypothyroidism.
>> Of course they don't.
>But note that Iodine deficiency is an important factor in thyroid
>disease, and the Japanese diet is Iodine-rich because of the large
>amount of shellfish and other seafood consumed. Perhaps that explains
>why thyroid disease is no more common here in Japan than in countries
>where soy is not eaten in similar quantities.

Sorry, but that's not it. Hypothyroidism is most common in Japanese
coastal areas where iodine intake is HIGHEST.

One of my beefs with the orthopathic weenies is that they simply
look at a problem and throw whatever nutrient they can think of at it.
Alas, iodine/iodide supplementation is useful only for one small
(now rare) kind of hypothyroidism. All the other kinds it does
either nothing for, or else causes it to get worse (since iodine
actually suppresses thyroid function at high doses). The last is
probaby what is happening in Japan with the Hashimoto's
disease-- there are a lot of people on the very edge of
clinical hypothyroidism as a result of autoimmune thyroid
distruction, and high iodine intake pushes them over the top.


From: "Steve Harris" <>
Subject: Re: Do Japanese develop hypothyroidism?
Date: Sat, 5 May 2001 00:34:46 -0600

"Quentin Grady" <> wrote in message
> This post not CC'd by email
>  On 2 May 2001 10:02:22 -0400, (Ron Roth) wrote:
> >x-no-archive: yes
> >
> >SH>Sorry, but that's not it. Hypothyroidism is most common in Japanese
> >SH>coastal areas where iodine intake is HIGHEST.
> >
> >SH>One of my beefs with the orthopathic weenies is that they simply
> >SH>look at a problem and throw whatever nutrient they can think of at it.
> >SH>Alas, iodine/iodide supplementation is useful only for one small
> >SH>(now rare) kind of hypothyroidism. All the other kinds it does
> >SH>either nothing for, or else causes it to get worse (since iodine
> >SH>actually suppresses thyroid function at high doses). The last is
> >SH>probaby what is happening in Japan with the Hashimoto's
> >SH>disease-- there are a lot of people on the very edge of
> >SH>clinical hypothyroidism as a result of autoimmune thyroid
> >SH>distruction, and high iodine intake pushes them over the top.
> >
> >--
> > Actually, it's the high bromine content (high Br/I ratio),
> > not high iodine from seafood/seaweed and other sources that
> > suppress the thyroid.  High iodine does NOT suppress thyroid
> > functions, but high bromine and (phyto)estrogenic sources do,
> > as they are thyroid/iodine antagonists.
> G'day G'day Ron and Steve,
>   Excess iodine ... excess bromine ... excessive Br/I ratio?
> Thanks for opening up these possibilities for discussion.  The next
> generation is going to be so much more knowledgeable than this one ...
> darn.  Just when we thought we were more knowledgeable than our
> parents along comes another generation.  <grin>
> > For the same reason, many hyperthyroid females start to develop
> > the problem as they approach menopause, And HRT or a number of
> > estrogen-supporting supplements are a simple fix for many of
> > these cases.  * Ron Roth
> Ron,  I apologize for not following the logic in the above paragraph.
> If phytoestrogen sources suppress thyroid function and women take
> these as supplements I'd have thought it would have made their thyroid
> sibilation worse.

Don't expect anything Ron says to make any sense.

Raw soy does have something in it which mildy raises thryoid hormone levels,
but it's not the chief isoflavone genistein. It's not clear what it is. For
a while they though the anticholesterol effect of soy was due to the
increase in thyroid hormone levels, but isolated soy protein lowers
cholesterol without raising T4 levels (unlike soy protein concententrate
which does both), so that's not it. It's still a mystery. In any case, this
is not an ANTI-thyroid effect, but rather a prothyroid one. There are
antithyroid soy products, but they are the fermented ones like miso, and the
villain there is probably a antithyroid fungal polyphenol called kojic acid.
But it's not an estrogen. Lord knows where Ron gets all these ideas, but
what he's telling you is all mixed up.

Yes, iodine is directly thyroid suppressive. Yes, high iodine areas in Japan
get more hypothyroidism. Ron seems to think this is bromine, but there's no
epidemiological evidence for it in Japan. You can make animals hypothyroid
with pharmacological doses of bromide, and there are some reports of this
happening to people, but it's not from any amount of bromine you could get
in a sea-based diet. This happens only at very unnatural levels of


J Clin Endocrinol Metab 1994 Feb;78(2):393-7

Association between dietary iodine intake and prevalence of subclinical
hypothyroidism in the coastal regions of Japan.

Konno N, Makita H, Yuri K, Iizuka N, Kawasaki K

Department of Internal Medicine, Hokkaido Central Hospital for Social Health
Insurance, Sapporo, Japan.

The prevalence of thyroid dysfunction in relation to iodine intake was
studied in adults (n = 1061) in five coastal areas of Japan that produce
iodine-rich seaweed (kelp). The prevalence of hyperthyroidism (TSH < 0.15
mU/L) was similar in these areas, whereas that of hypothyroidism (TSH >
5.0 mU/L) varied from 0-9.7%. The relative frequency of above normal
iodide concentration in the morning urine (> or = 75 mumol/L) [high
urinary iodide (UI)] varied from 3.7%-30.3%. Together with previously
reported results of a noncoastal city, the frequency of high UI
correlated significantly with that of hypothyroidism with negative
thyroid autoantibody (r = 0.829, n = 6, P < 0.05) but not with positive
thyroid autoantibody (r = 0.278, NS) or with that of hyperthyroidism (r =
0.038, NS). Hypothyroidism was more prevalent in thyroid
autoantibody-negative subjects with high UI (group II, 12.1%) than with
normal UI (group I, 2.3%) (P < 0.001).  The TSH [21.9(6.5-73.7)mU/L]
(mean +/- SD) and thyroglobulin [288 (182-456) micrograms/L] levels in
group II were significantly higher than the respective levels in group I
[9.6(3.7-25.3)mU/L and 123 (38-399) micrograms/L] (P < 0.05).  Free T4 of
group II (9.9 +/- 3.9 pmol/L) was significantly lower than in group I
(14.2 +/- 3.9 pmol/L) (P < 0.05). These results indicate that 1) the
prevalence of hypothyroidism in iodine sufficient areas may be associated
with the amount of iodine ingested; 2) hypothyroidism is more prevalent
and marked in subjects consuming further excessive amounts of iodine; and
3) excessive intake of iodine should be considered an etiology of
hypothyroidism in addition to chronic thyroiditis in these areas.

PMID: 8106628

Clin Endocrinol (Oxf) 1993 Mar;38(3):273-81

Screening for thyroid diseases in an iodine sufficient area with sensitive
thyrotrophin assays, and serum thyroid autoantibody and urinary iodide

Konno N, Yuri K, Taguchi H, Miura K, Taguchi S, Hagiwara K, Murakami S

Department of Medicine, Hokkaido Central Hospital for Social Health
Insurance, Sapporo, Japan.

OBJECTIVE: The present study was designed to investigate the prevalence
of thyroid dysfunction and its relation to thyroid autoantibodies and
urine iodide concentration in apparently healthy people residing in
Sapporo, a city of northern Japan, where the iodine intake is high.
DESIGN AND SUBJECTS: Serum TSH and thyroid autoantibodies, and urine
iodide were measured in 4110 people (2931 men and 1179 women) (age 45.6
+/- 10.3 years (mean +/- SD)) who were recruited at the hospital for
medical examinations. RESULTS: The thyroid autoantibodies were positive
in 6.4% of males and 13.8% of females with an age-related increase. Of
the people with positive antibodies, 87.2% had normal TSH values
(0.15-5.0 mU/l) as measured by a sensitive assay. The prevalence of
unsuspected hyperthyroidism as defined by suppressed TSH values was
0.61%, of which 64% was diagnosed as Graves' disease based on positive
thyrotrophin receptor antibody results. The prevalence of unsuspected
hypothyroidism, as evidenced by supranormal TSH, was 0.68% for males and
3.13% for females with an age-related increase. Of those with
hypothyroidism, 45.5% were autoantibody positive.  The overall prevalence
of Hashimoto's thyroiditis was 13.11% for females and 6.15% for males.
The urine iodide levels of hypothyroidism with a positive autoantibody of
38.5 (17.7-83.9) mumol/l and a negative autoantibody of 34.9 (17.9-67.9)
mumol/l were both significantly higher than that of normal subjects (26.9
(14.6-49.6) mumol/l) (P < 0.01). When iodine intake was restricted for
6-8 weeks for hypothyroid subjects, the elevated TSH and thyroglobulin
and low free T4 levels were reversed in the autoantibody negative but not
in the positive group. CONCLUSIONS: This study provides further
information on the prevalence of thyroid dysfunction and autoimmune
thyroid diseases in an iodine sufficient area. In addition, it suggests
that more than half of the patients with unsuspected hypothyroidism were
negative for autoantibodies and that the excessive iodine intake may be
involved in causing latent hypothyroidism.

PMID: 8458099

Nephron 1993;65(1):51-5

Iodine-induced hypothyroidism in patients on regular dialysis treatment.

Takeda S, Michigishi T, Takazakura E

Kurobe City Hospital Toyama, Japan.

Hypothyroidism with a serum concentration of thyroid-stimulating hormone
(TSH) above 40 microU/ml was noted in 3 (3.2%) of 93 patients on regular
hemodialysis or continuous ambulatory peritoneal dialysis. These 3
patients had no history of thyroid disease and were receiving no
medication known to influence thyroid function. They had habitually eaten
iodine-rich foods and showed an enlarged thyroid gland with a preserved
radioactive iodine uptake and a markedly elevated serum inorganic iodine
(II) level. In all 3 patients, both thyroidal microsomal antibody and
thyroglobulin antibody titers measured by hemagglutination methods were
less than 100, and TSH-binding inhibitory immunoglobulin was negative.
Moreover, histologically no lymphocytic infiltrations were observed. With
only iodine restriction, serum TSH level markedly decreased from 44.6 to
3.6 microU/ml in case 1, from 90.6 to 3.2 microU/ml in case 2 and from
43.2 to 9.4 microU/ml in case 3 in parallel with decreases in the serum
II level. These results suggest that at least in an area like Japan,
where the daily intake of iodine is high, iodine-induced hypothyroidism
may be induced in patients undergoing regular dialysis treatment even in
the absence of apparent underlying thyroid disease.

PMID: 8413791

Baillieres Clin Endocrinol Metab 1988 Aug;2(3):591-617

Autoimmunity and hypothyroidism.

Amino N

Hypothyroidism can be induced by various diseases. An autoimmune cause
accounts for approximately 90% of adult hypothyroidism, mostly due to
Hashimoto's disease. The majority of Hashimoto patients are women aged
between 20 and 60 years old and nearly 10% show overt hypothyroidism.
With time euthyroid patients progress to hypothyroidism and thus the
prevalence of hypothyroidism is higher in elderly patients. Especially at
3 to 8 months postpartum, the prevalence of hypothyroidism is very high,
up to 2-4%, but more than 90% of these cases are transient. Autoimmune
destructive mechanisms, such as antibody dependent cytotoxicity, K and NK
cell cytotoxicity, T lymphocyte cytotoxicity and lymphokine cytotoxicity,
have been studied in vitro, but the most important factor in vivo is
still unknown. A recent finding is that thyroid stimulation blocking
antibody (TSBAb) may induce primary atrophic hypothyroidism. This
antibody not only blocks TSH-induced cAMP production but also blocks
TSH-induced DNA synthesis and iodine uptake in cultured thyroid cells.
The prevalence of TSBAb in patients with primary atrophic hypothyroidism
varies in different studies, from 0 to 47%. Reports on the relationship
between TSBAb and TSH-binding inhibitory immunoglobulin (TBII) detected
by radioreceptor assay are conflicting. The prevalence of TSBAb in
patients with goitrous hypothyroidism is also controversial, varying from
0 to 20%. Transient hypothyroidism is observed frequently in the
postpartum period and in the post-thyrotoxic phase of pregnancy-unrelated
silent thyroiditis. Maternal TSBAb causes transient neonatal
hypothyroidism when the activity is more than 1500 i.u./litre. The
blocking and stimulatory types of anti-TSH receptor antibodies may both
react with the same epitope(s) of TSH-receptor related antigens but the
exact mechanisms that lead to the different effects are unknown. In some
patients, including those with Graves' disease, stimulating and blocking
antibodies co-exist and thyroid function may change from hyperthyroidism
to hypothyroidism, or vice-versa, depending on the balance of stimulatory
and blocking activities.  Hypothyroidism in Graves' disease after
treatment is thought to be induced in two ways:  autoimmune thyroid
destruction and the predominant appearance of TSBAb.  Dietary iodine
restriction is helpful in allowing recovery from hypothyroidism in more
than half of the patients with spontaneously occurring primary
hypothyroidism in Japan. Submaximal doses of T3 may be useful in
differentiating transient from persistent hypothyroidism, since
spontaneous recovery is detected by an increase of serum T4.(ABSTRACT

Publication Types:
Review, tutorial

PMID: 3066320

Ann Clin Lab Sci 1976 Nov-Dec;6(6):545-50

Iodine induced thyroid disease.

Weaver DK, Nishiyama RH, Batsakis JG

Although iodine prevents goiter,enlarged thyroid glands continue to be
detected in subjects, especially children, in spite of adequate iodine
ingestion.  Iodine may cause goiter in susceptible individuals by
inhibiting the organic binding of iodine as is seen in adult asthmatics,
neonates born of iodine ingesting mothers and in subjects residing along
the littoral of Japan. Myxedema, especially in treated Graves' disease
and Hashimoto's disease, may also be precipitated by iodine. On the other
hand, iodine given to euthyroid subjects in areas of endemic goiter and
to subjects with nontoxic nodular goiter may induce thyrotoxicosis by
disclosing diffuse autonomously functioning thyroid tissue. An indirect
adverse effect of iodine upon the thyroid gland may be manifested by
lymphocyte glandular infiltrates and chronic thyroiditis which were
sparse or absent in thyroid glands removed from subjects living in iodine
deficient areas before iodine prophylaxis and therapy. Not only has the
incidence of thyroiditis increased, but the histologic and clinical
distinctions between treated Graves' disease and chronic thyroiditis have
become indistinct. Experimentally, chronic thyroiditis has been produced
in animals following large doses of iodine.  Accumulated evidence
supports the concept that iodine contributes to the genesis of chronic

PMID: 999225

From: Steve Harris <>
Subject: Re: Iodine content of foods
Date: 20 Jul 2005 18:25:18 -0700
Message-ID: <>

Michelle Guy wrote:
> Hi I am new to the group so if there is a FAQ please point me to it.
> I am interested in the iodine content of certain foods, as I have to
> avoid them (thyroid treatment). Particularly i am interested in Quorn
> or Mycoprotein.
> Thanks
> Michelle
> Michelle Ozzie in  Switzerland
> 70.4/71/60 Starting again 24.11.04


Look, you're not on an iodine restricted diet for any good medical
reason UNLESS it's a temporary thing as they're preparing to give you
radioiodine. Temporary is the key. And in which case the doc preparing
to do it should have provided you with a low iodine diet. Why not eat

If you really can't figure out how much iodine you're getting from
exotic foods you simply MUST continue to eat, then you can always have
your doc do a urine iodine test. That's a pretty good index of whether
or not you're getting so much iodine from food sources as to intefere
with radioiodine treatment.


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