Ray Peat Email Advice Depository

[windinthepines]

[2013]

Me:
Hi, I started used cyproheptadine for my insomnia and bowel problems. I used 1mg the first night, and it made me very sleepy. Now I'm using 4mg without any effect on sleep. Is there a safe upper dose?

RP:

I think it's best to use a minimal dose for a few days to see what its effect is on the digestive system, before trying bigger doses.

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

Me:

[I've had bad eczema for a long time.]

RP:

One of thyroid's important effects is the regulation of minerals, but its effects are limited by diet. How often have you been
eating liver and shell fish, and how much milk do you average? Do you drink coffee?

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

Me:


I was wondering if I'm thinking along the right lines: Blake was
describing some of the ways our culture and mentalities have gotten
stuck into rigid dimensions, so that we make a lot of mistakes based
on our faulty perception of the real world. By analyzing biological
research, you have worked out the biological mechanisms for our
mistaken outlook.

I was thinking about my own developing views, and how they've changed
dramatically in the last few years. I think that my changing diet and
other things were mostly responsible, allowing my substance to change
to accommodate new insights and see what I didn't see before. Do other
people tell you similar things?

RP:

I occasionally hear that when people start using thyroid or progesterone.

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


Me:

Hi Ray,

I got some lisuride to try. The pills have 200mcg each. When I was
using Stablon, I liked how it made me feel optimistic, and ready for
opportunities and adventure, but I didn't like the brain-fogged
feeling from using it everyday. So far, using lisuride sporadically, I
haven't noticed much from it. Is there a good way to use lisuride? I
thought that it would be good to use it more like LSD, in little doses
every few weeks.

RP:

I think occasional use would be better. Have you used pregnenolone or cyproheptadine?

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

Me:
[Question about chocolate and cottage cheese]

RP:

Part of the value of chocolate was the fat, but it's more profitable to sell it as a pharmaceutical, so they
substitute PGPR, which was a cheap polymer used as a well-drilling lubricant. There's a national brand
of cottage cheese that (so far) hasn't been using the toxic "cultures," Kalona's Super Natural.

Me:

Thanks for that PGPR information. Kolona's Super Natural lists
cultures on the ingredient list. Is that different from the cultured
milk that the Daisy brand uses?

RP:

Yes, I've heard bad reports on the Daisy, nothing but good results with Kalona.

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

Me:

[Pork rinds?]

RP:

I soak mine in hot coconut oil and then drain them, to exchange some of the fat.

 

[windinthepines]

[2012]

Me:

[Sent a poem I wrote about goats.]

RP:

Thanks. I don't remember the context, but it's a good image for reconsidering the world. Have you read any of Peter Kropotkin? Here's a nice quotation from him:

Then the peasants of the little Belgian village, Gheel, found something better. They said: "Send us your insane. We will give them absolute freedom." They adopted them into their families, they gave them places at their tables, chance alongside them to cultivate their fields and a place among their young people at their country balls. "Eat, drink, dance with us. Work, run about the fields and be free." That was the system, that was all the science the Belgian peasant had. And liberty worked a miracle. The insane became cured.[...] The cures were attributed to a saint and virgin. But this virgin was liberty and the saint was work in the fields and fraternal treatment.

Me:

I think Sarah on KMUD was asking you about an easy way for everyone to get milk: either a cow in every yard, or a goat on every roof, in the city. Thanks for that Kroptkin quote, it's perfect. It reminds me of an article I saw about how schizophrenics do better in poorer nations, like India, where they aren't isolated in hospitals, remaining instead in family and community life. I'll have to read Kroptkin now. I'm just starting to read more Blake, and am finding your Blake essay to be a wonderful introduction to him. In his writing I keep finding ideas I've already encountered in your work. When I studied literature in college, the professors always denied that fiction writers were trying to communicate something, treating the books instead as "texts," or cultural relics without intrinsic meaning--of course they often seemed to chose books where that really was the case.

RP:

I haven't been around the literature people for a long time, but I knew that sort of thing was happening. You can read about how that bizarre attitude toward culture was created by the Congress for Cultural Freedom (i.e., the CIA) in Frances Saunders' book and many good articles by Richard Cummings. I first heard about it in an article by Siqueiros, who called it the "ghost art" created by the Rockefellers, but then the CIA financing (using money from the Marshall Plan for reconstructing Europe) was revealed.

Tony Papert:
"For readers of Frances Stonor Saunders’ Who Paid the Piper, a history of the Congress for Cultural Freedom (CCF), or of the 1967 expose ́s by Ramparts and then by Tom Braden, the answer is unavoidable: Beginning in the early 1950s, an avalanche of U.S. taxpayers’ money “covertly” subsidized this particular school, to the exclusion of all else. EIR and others have described the long and lavish arts festivals put on in Paris and other war-ruined European cities, but it is equally true,- even if it is illegal,—that the “CIA” massively funded its chosen artistic styles in the United States as well. Think of the Museum of Modern Art continually on world tour, courtesy of the CCF, with the works of its chosen abstract expressionist painters; the Boston Symphony Orchestra likewise, with its chosen composers, and so on."

 

[windinthepines]

[2012]

Me:

Dr Peat,

Over the years, have you seen a change in the the types of health
problems people have? I get the sense from your books and older
articles that pregnenolone was able to cure a lot of people's
problems. But I haven't heard any recent stories about big
improvements from pregnenolone. Do people today have very different
metabolisms than people did just a few decades ago? A chart I saw
showed an average increase of 10 grams of PUFA per day just since
1999. People my age (20s) and younger also don't eat much protein,
maybe for cultural reasons, or low appetites.

RP:

Besides the average change in diet, people now have a more complete set of expectations about their health, and the substances used in supplements have changed. Many people expect pregnenolone to act like a hormone, which it doesn't; I've only seen a couple of people younger than their late 40s who felt anything at all from it. And a single dose is often all it takes, and continued, or bigger, doses don't do anything more.


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

Me:

[Low DHEA]

RP:

It's important to get the nutrients in balance--both zinc and vitamin A are involved in the conversion, and will tend to be
depleted when the metabolic rate is higher.

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

Me:

[Where is good aspirin?]

RP:

I know people who get the pure (USP or BP) aspirin from a chemical company in India, or from veterinary stores in the US.

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

Me:

I was curious about the colors in the paintings on your website,
especially the blue that sick women can have. It seems to me like the
hormonal state of the women you're painting seeps into their
surroundings. I've started to notice that the way I feel can
dramatically change the way I perceive the world around me--is that
something you're intending in your paintings?

RP:
Yes, tangentially thinking about the effects of colors.

Me:

I think you have the best writing style I've come across. What sort of
writers or poets do you like, aside from Blake? Any of the beat
writers?

RP:

Thanks. Yes, I liked the style of several of the beat writers, Kerouac's fluidity, and Ginsberg's more intense confrontation of the culture. Aldous Huxley was another person strongly influenced by Blake.

Me:

I like Kerouac, Ginsberg and Huxley a lot too. It's interesting you
mention Kerouac's fluidity: I read he wrote the first few pages of On
the Road in French, and I always wondered how his French influenced
his English style. Sometimes your style reminds me of Ivan Illich's,
because he didn't seem to write with cliches either. Do you read in a
lot of languages?

RP:

I felt that my school English classes had given the language a sense of artificiality for me. When I first saw verses by Blake I realized that was how English should work; later, I saw that the Beats were reclaiming English. When I was in Mexico, an American student commented that when I spoke English I sounded depressed, but that I sounded happy when I was speaking Spanish. I think that was because I learned it just by listening and talking to people in Mexico City, and so it contained my feelings about those experiences. My projects were very similar to Illich's, freeing ourselves from the culture's stereotypes. (I was often in Mexico between 1955 and 1965, overlapping Illich's time there. I had Blake College there in the early '60s.) The only other languages I read often are French and Italian; oddly, reading French feels more efficient than reading English, probably because I've never spoken it.

Me:

I don't know if he read Blake, but for me Henry Miller can write
English in the right way too. Blake College sounds like the type of
school I'd like to have gone to. I read a little about it in the book
Ungodly about Madelyn Murray O'Hair. Is there anywhere else to read
about it? Or do you happen to know if there are any similar schools
today?

RP:

There were some newspaper and magazine articles about it in the 'sixties, but not much.
In 1965 I knew someone with a friend in the Mexico City branch of the Ford Foundation, and we submitted a proposal to them for funding. Right after the Madalyn events, I learned that they were funding an experimental, student centered college at Fordham University, and I think other places; the foundation and the government worked closely together, and I think they saw the importance of co-opting the movement, to keep it from getting too independent, i.e., anti-imperialist. I think our idea of giving a diploma whenever the person scored very high on the Graduate Record Exam, which would let them get into good graduate study programs, was the main point they wanted to suppress, since it eliminated all of the judgmental points of control in the process.

 

[windinthepines]

[2012]

Me:

If someone is avoiding PUFAs carefully for a few years, is there any
way to tell if they've gotten rid of most of their stored PUFA? I was
thinking maybe if they let themselves get hungry, they would feel
different than someone who is releasing PUFA.

RP:

The resting metabolic rate will be higher, and there will be less tendency to have inflammation after an injury. Although they have to eat more calories, I think they don't experience the intense stress from hunger.

Me:

In one of your newsletters you wrote about the experimenter who tried
to induce an EFA deficiency in himself by eating a fat free diet, and
I thought it only took him six months to see benefits, rather than
three or four years. Did eating a fat free diet allow him to reduce
his PUFA stores more quickly?

RP:

He saw benefits after only about 3 months, but we don't know what would have happened as his tissue stores were depleted. The animal evidence implies that there would be tremendous resistance to stress and inflammation.


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

Me:

[...] Can we absorb vitamin E topically?

RP:

Yes, that's how I use it.

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

Me:

When I wake up sometimes, my hands feel very week. If I clench my
fist, I can feel that my grip strength is very weak. I'd thought this
was a sign of a high reverse T3. Or could it mean I ran out of
glycogen during the night?

RP:
I think it's a combination of glycogen and various hormones; the nervous system takes a while to wake up fully.


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

Me:

[Vitamin A question]

RP:

Yes, all the synthetic vitamin A that I've tried was too allergenic for me to use orally, but I don't react to it on the skin. I know people who have systemic allergic responses to some water soluble vitamins on their skin, but you're the first I've heard reacting that way to A.

Me:

I was surprised to hear that depression can be an allergic symptom.
I'm used to getting an itchy feeling on my skin from some supplements
and foods, but this is the first supplement I've gotten this sort of
reaction from. I still have dandruff and pimples, so I don't think I'm
getting too much vitamin A, especially since I only used one drop of
the vitamin. Can too much vitamin A lead to acne and dandruff too?

RP:

Yes, but I've never heard of it with less than 50,000 units a day. An extreme vitamin E deficiency predisposed to A toxicity.

Me:

Do you think it might be worth trying a vitamin E supplement?

RP:

If you have eaten much unsaturated fat in recent years, your requirement for vitamin E is probably high.

Me:

[Keloids related to Vitamin E?]

RP:

Yes, a deficiency of E does seem to be a factor in keloids. Do you eat liver?

Me:

[Yes]

RP:

The full range of nutrients in liver is much better than a single supplement.

 

[windinthepines]

[2011]

RP:

Extra iodine could make a thyroid problem worse, though if there are breast cysts it might help them temporarily.

Endocr Pathol. 2002 Fall;13(3):175-81.
Thyroid cancer and thyroiditis in Salta, Argentina: a 40-yr study in relation to iodine prophylaxis.
Harach HR, Escalante DA, Day ES.
Services of Pathology, Dr A Oñativia Endocrinology and Metabolism Hospital,
Salta, Argentina. [email protected]
The natural history of thyroid cancer and thyroiditis in relation to iodine
prophylaxis in the region of Salta, Argentina, where goiter is common was
investigated over a time span of 40 yr. For analysis of thyroid cancer, the
specimens were divided into two periods. The first 15 yr (59 cases), including 5
yr before prophylaxis, was compared with the second 25 yr (182 cases), a period
well after salt iodination. Papillary carcinomas formed the largest group of
tumors in both periods, with a significant increase in their proportion in the
second period (44 vs 60%, chi(2): p < 0.05), while the percentage of follicular
and undifferentiated carcinomas decreased and medullary carcinoma remained about
the same. The ratio of papillary to follicular carcinoma rose from 1.7:1 in the
first period to 3.1:1 in the second. Four thyroid lymphomas of non-Hodgkin's
B-cell type occurred in the second period in females over age 50. A severe
lymphoid thyroiditis was present in the two cases with assessable background
thyroid tissue. The frequency of moderate to severe lymphoid infiltrate in
females rose from 2 of 12 (16.6%) in the preprophylaxis period to 34 of 114
(28.0%) in the last 25 yr after prophylaxis. After salt prophylaxis, thyroiditis
was more frequent in patients with papillary carcinoma (36.2%) than in those with
nonpapillary tumors (14.7%) (chi(2), p < 0.02). These observations indicate that
a high dietary intake of iodine may be associated with a high frequency of
papillary carcinoma and thyroiditis, and that thyroiditis is more commonly
associated with papillary carcinoma than with other thyroid tumors. The
occurrence of non-Hodgkin's lymphomas only in the postprophylaxis period may be
linked to an increase in thyroiditis.

J Endocrinol Invest. 2003;26(2 Suppl):49-56.
Iodine excess and thyroid autoimmunity.
Bournaud C, Orgiazzi JJ.
Service d'Endocrinologie, Diabétologie et Maladies Métaboliques, Centre
Hospitalier Lyon-Sud, 69495 Pierre-Bénite Cedex, France.
Epidemiological studies, as well as animal models, indicate that iodine might be
an immunogenic agent for the thyroid gland, at least in subjects predisposed to
thyroid autoimmunity. This review presents data, either epidemiological or
experimental, obtained in different conditions: constant and stable iodine
status, either deficient, sufficient or excessive; long-term iodine prophylaxis;
temporary supplementation with iodide (6-12 months) or iodised oil. Moreover, we
also discuss data obtained in the general population, among subjects with
euthyroid goiter, or autoimmune goiter, or even in women prone to post-partum
thyroid diseases. It is concluded that the significant increase in the prevalence
of autoimmune thyroid diseases in populations living in iodine sufficient areas
should not prevent the implementation of the iodine prophylaxis.

J Immunol. 2002 Jun 1;168(11):5907-11.
Enhanced iodination of thyroglobulin facilitates processing and presentation of a
cryptic pathogenic peptide.
Dai YD, Rao VP, Carayanniotis G.
Division of Endocrinology, Faculty of Medicine, Memorial University of
Newfoundland, St. John's, Newfoundland, Canada.
Increased iodine intake has been associated with the development of experimental
autoimmune thyroiditis (EAT), but the biological basis for this association
remains poorly understood. One hypothesis has been that enhanced incorporation of
iodine in thyroglobulin (Tg) promotes the generation of pathogenic T cell
determinants. In this study we sought to test this by using the pathogenic
nondominant A(s)-binding Tg peptides p2495 and p2694 as model Ags. SJL mice
challenged with highly iodinated Tg (I-Tg) developed EAT of higher severity than
Tg-primed controls, and lymph node cells (LNC) from I-Tg-primed hosts showed a
higher proliferation in response to I-Tg in vitro than Tg-primed LNC reacting to
Tg. Interestingly, I-Tg-primed LNC proliferated strongly in vitro against p2495,
but not p2694, indicating efficient and selective priming with p2495 following
processing of I-Tg in vivo. Tg-primed LNC did not respond to either peptide.
Similarly, the p2495-specific, IL-2-secreting T cell hybridoma clone 5E8 was
activated when I-Tg-pulsed, but not Tg-pulsed, splenocytes were used as APC,
whereas the p2694-specific T cell hybridoma clone 6E10 remained unresponsive to
splenic APC pulsed with Tg or I-Tg. The selective in vitro generation of p2495
was observed in macrophages or dendritic cells, but not in B cells, suggesting
differential processing of I-Tg among various APC. These data demonstrate that
enhanced iodination of Tg facilitates the selective processing and presentation
of a cryptic pathogenic peptide in vivo or in vitro and suggest a mechanism that
can at least in part account for the association of high iodine intake and the
development of EAT.

Thyroid. 2001 May;11(5):501-10.
Iodine-Induced hypothyroidism.
Markou K, Georgopoulos N, Kyriazopoulou V, Vagenakis AG.
Department of Medicine, University of Patras Medical School, Greece.
Iodine is an essential element for thyroid hormone synthesis. The thyroid gland
has the capacity and holds the machinery to handle the iodine efficiently when
the availability of iodine becomes scarce, as well as when iodine is available in
excessive quantities. The latter situation is handled by the thyroid by acutely
inhibiting the organification of iodine, the so-called acute Wolff-Chaikoff
effect, by a mechanism not well understood 52 years after the original
description. It is proposed that iodopeptide(s) are formed that temporarily
inhibit thyroid peroxidase (TPO) mRNA and protein synthesis and, therefore,
thyroglobulin iodinations. The Wolff-Chaikoff effect is an effective means of
rejecting the large quantities of iodide and therefore preventing the thyroid
from synthesizing large quantities of thyroid hormones. The acute Wolff-Chaikoff
effect lasts for few a days and then, through the so-called "escape" phenomenon,
the organification of intrathyroidal iodide resumes and the normal synthesis of
thyroxine (T4) and triiodothyronine (T3) returns. This is achieved by decreasing
the intrathyroidal inorganic iodine concentration by down regulation of the
sodium iodine symporter (NIS) and therefore permits the TPO-H202 system to resume
normal activity. However, in a few apparently normal individuals, in newborns and
fetuses, in some patients with chronic systemic diseases, euthyroid patients with
autoimmune thyroiditis, and Graves' disease patients previously treated with
radioimmunoassay (RAI), surgery or antithyroid drugs, the escape from the
inhibitory effect of large doses of iodides is not achieved and clinical or
subclinical hypothyroidism ensues. Iodide-induced hypothyroidism has also been
observed in patients with a history of postpartum thyroiditis, in euthyroid
patients after a previous episode of subacute thyroiditis, and in patients
treated with recombinant interferon-alpha who developed transient thyroid
dysfunction during interferon-a treatment. The hypothyroidism is transient and
thyroid function returns to normal in 2 to 3 weeks after iodide withdrawal, but
transient T4 replacement therapy may be required in some patients. The patients
who develop transient iodine-induced hypothyroidism must be followed long term
thereafter because many will develop permanent primary hypothyroidism.

Saudi Med J. 2007 Jul;28(7):1034-8.
The effect of iodine prophylaxis on the frequency of thyroiditis and thyroid
tumors in Southwest, Iran.
Soveid M, Monabbati A, Sooratchi L, Dahti S.
Department of Internal Medicine, Shiraz University of Medical Sciences, Nemazee
Hospital, Shiraz, Iran. [email protected]
OBJECTIVE: To investigate the effect of the salt iodization program, which was
initiated in 1989 on frequencies of thyroiditis and papillary carcinoma in Fars
province of Iran, which was previously an iodine deficient area. METHODS: Four
hundred and eighty-two thyroidectomy specimens belonging to the pre-iodization
period from 1983 to 1988, and 466 post iodization specimens from 1998 to 2003
were re-examined for presence of lymphocytic infiltration and types of thyroid
tumors. This study was carried out in Shiraz University of Medical Sciences,
Iran. RESULTS: The frequency of lymphocytic infiltration in non-neoplastic
specimens increased from 30-60.5% after salt iodization (p<0.001). Background of
lymphocytic infiltration in neoplastic specimens also increased from 18.5-61%
after iodine prophylaxis (p<0.001). The frequency of papillary carcinoma in
neoplastic specimens increased from 15-43% (p=0.01) and that of follicular
adenoma decreased from 69-32.5% (p<0.0001). CONCLUSION: Salt iodization is
associated with an increased occurrence of histologic thyroiditis and papillary
carcinoma.

Biol Trace Elem Res. 2007 Oct 20 [Epub ahead of print]
Safe Range of Iodine Intake Levels: A Comparative Study of Thyroid Diseases in
Three Women Population Cohorts with Slightly Different Iodine Intake Levels.
Teng X, Shi X, Shan Z, Jin Y, Guan H, Li Y, Yang F, Wang W, Tong Y, Teng W.
Department of Endocrinology and Metabolism, The First Affiliated Hospital, China
Medical University, No. 155 Nanjing Bei Street, Heping District, Shenyang,
Liaoning Province, 110001, People's Republic of China, [email protected].
Iodine excess may lead to thyroid diseases. Our previous 5-year prospective
survey showed that the prevalence and incidence of hypothyroidism or autoimmune
thyroiditis increased with iodine intake. The aim of the present study was to
investigate the optimal range of iodine intake by comparing the prevalence of
thyroid diseases in three areas with slightly different levels of iodine intake.
In 2005, 778 unselected women subjects from three areas with different iodine
intake levels were enrolled. Levels of serum thyroid hormones, thyroid
autoantibodies, and urinary iodine were measured, and thyroid B ultrasounds were
performed. Among the subjects with mildly deficient iodine intake, those with
adequate intake, and those with more than adequate intake, the prevalence of
clinical and subclinical hypothyroidism was 0, 1.13, and 2.84%, respectively (P =
0.014); that of thyroid goiter was 24.88, 5.65, and 11.37%, respectively (P <
0.001); that of serum thyrotropin values was1.01, 1.25, and 1.39 mIU/l,
respectively; and that of serum thyrotropin/thyroglobulin ratio was 7.98, 6.84,
and 5.11, respectively (P < 0.001). In conclusion, median urinary iodine 100~200
mug/l may reflect the safe range of iodine intake levels. Serum
thyrotropin/thyroglobulin ratio might be a better index of evaluating iodine
status.

Endocrinology. 2007 Jun;148(6):2747-52. Epub 2007 Mar 8.
Induction of goitrous hypothyroidism by dietary iodide in SJL mice.
Li HS, Carayanniotis G.
Faculty of Medicine, Memorial University of Newfoundland, St. John's,
Newfoundland, Canada.
Prolonged intake of large amounts of iodide has been reported to increase the
incidence of goiter and/or hypothyroidism in humans as well as animals prone to
spontaneous autoimmune thyroiditis. In the current study, we investigated the
role of dietary iodide on the development of hypothyroidism, as well as
thyroiditis, in strains of mice that do not develop spontaneous autoimmune
thyroiditis. Intake of 0.05% NaI via drinking water for 10 wk induced
hypothyroidism in SJL/J mice as indicated by elevated TSH and depressed total
T(4) values in serum and formation of colloidal goiter with an inactive flattened
thyroid epithelium. Hypothyroidism did not appear to have an autoimmune basis
because only focal mononuclear cell infiltrates were found intrathyroidally, and
antithyroglobulin antibodies or increased organification of iodide were not
detected. These phenomena were not observed in similarly treated CBA/J mice,
suggesting polymorphisms in genes controlling events downstream of iodide uptake
by thyrocytes. Interestingly, RT-PCR analysis indicated that unlike CBA/J, SJL/J
mice could not down-regulate Na/I symporter gene expression during the NaI
treatment. No significant temporal or strain differences were observed regarding
the expression of thyroglobulin, pendrin, thyroid peroxidase, and DUOX1 and DUOX2
genes after NaI intake. Our results point to the generation of a mouse model for
the study of iodine-induced hypothyroidism, which does not seem to have an
autoimmune basis.

J Endocrinol Invest. 2007 Apr;30(4):274-8.
Urinary iodine excretion and antiperoxidase enzyme antibody in goitrous and
healthy primary school children of Arak, Iran.
Rezvanfar MR, Farahany H, Chehreiy A, Nemati M, Rostamy S, Karimy E.
Division of Endocrinology, Department of Internal Medicine, Arak Medical Science
University, Arak, Iran. [email protected]
OBJECTIVE: To determine urinary iodine excretion (UIE) and antiperoxidase enzyme
antibody (anti-TPO Ab) in primary school-age children living in Arak, Iran, in
2005, after 10 yr of iodized salt distribution in an effort to ameliorate iodine
deficiency. METHODS: Through an observational, case-control study and by means of
satisfied sampling, 6520 primary school children were examined for goiter, and
then 193 goiterous children (case) and 151 healthy (control) children were
assessed as representative samples for thyroid function tests, antiperoxidase
antibody, and urinary iodine excretion. Normal values of anti-TPO Ab were <40
U/ml and high values >75 U/ml. Normal values of urinary iodine concentration were
> or =10.0 microg/dl, and severe iodine deficiency were <2 microg/dl. The data
were analyzed and compared by the Chi- Square tests and Mann-Whitney U in SPSS
software; p-values <0.05 were considered statistically significant. RESULTS:
Total mean prevalence of goiter was 5.2%, ranging from 3.6 to 6.4% in different
schools. The prevalence of goiter increased with age; it was 3% in children aged
6-7 yr and 6.3% in children aged 11 yr (p<0.001). Mean iodine urinary
concentration was 16.36 microg/dl (+/-1.58). No difference was seen between the
mean urinary iodine in girls (17.30+/-3.80 micorg/dl) and boys (15.72+/-2.72
microg/dl). No difference was seen between the mean urinary iodine in goiterous
and healthy school children (17.4+/-3.7 microg/dl vs 15.3+/-3.18 microg/dl,
p=0.78). About 49.5% of school children had UIE<10 microg/dl and 28% had UIE<5
microg/dl. High levels of anti-TPO Ab were found in 21 school children (18
goiterous vs 3 healthy children, p=0.01) resulting in a total prevalence of 6.1%.
In females, the prevalence was 1.3 times higher than in males (male:female ratio
3/4). Thirteen out of 21 (62%) children with positive antibodies had significant
goiter (grade 2), and 5 (24%) had small goiter (grade 1), whereas only 3 children
(14%) had normal thyroid size (p=0.001). CONCLUSION: If urinary iodine
concentration is considered an index of total body iodine content, this study
demonstrated that prolonged iodized salt intake has minimized the occurrence of
iodine deficiency goiter and now autoimmune thyroid enlargement is one cause for
continuous goiter in primary school children, although there are unknown
etiologies that need to be considered in further studies.

Zhonghua Fu Chan Ke Za Zhi. 2003 Apr;38(4):216-8.
[Prevalence of postpartum thyroiditis in three different iodine intake areas]
[Article in Chinese]
Li D, Li CY, Teng WP.
Department of Obstetrics and Gynecology, Shenyang Fourth Peoples' Hospital,
Shenyang 110032, China.
OBJECTIVE: To investigate the prevalence of postpartum thyroiditis (PPT) in three
different iodine intake areas, to explore the relationship between iodine intake
and PPT. METHODS: Panshan, Zhangwu and Huanghua are three different iodine intake
areas. The median urinary iodine concentration were 103 micro g/L, 374 micro g/L
and 614 micro g/L, respectively. One hundred and nineteen lactational women were
investigated during the first year postpartum. Thyroid stimulating hormone (TSH),
free thyroxine (FT(4)), free triiodothyronine (FT(3)), thyroid peroxidase
antibody (TPOAb) and thyroglobulin antibody (TGAb) were determined with immulite
method, and UI was determined by As-Ce(4+) catalytic spectrophotometry method.
RESULTS: The prevalence of PPT is 11.8%, 10.1% of subclinical PPT, whereas 1.7%
of clinical PPT. There was statistically significant difference in the frequency
of PPT in three areas (Panshan 5.6%, Zhangwu 23.1% and Huanghua 6.8%, P < 0.05),
but no difference in the frequency of thyroid autoimmune antibody (TAA). 50% of
positive TAA women developed into PPT. CONCLUSION: Higher prevalence of
subclinical PPT was found in the area with moderate iodine deficiency after
iodine supplementation, suggesting a possible role of iodine supplementation in
PPT.

J Endocrinol Invest. 2005 Nov;28(10):876-81.
High iodine intake is a risk factor of post-partum thyroiditis: result of a
survey from Shenyang, China.
Guan H, Li C, Li Y, Fan C, Teng Y, Shan Z, Teng W.
Department of Endocrinology, the First Hospital Affiliated to China Medical
University, Shenyang, Liaoning Province, P.R. China.
The aim of the present study is to obtain the epidemiological data on post-partum
thyroiditis (PPT) firstly in Chinese women, and to tryto evaluate whether
excessive intake of iodine in post-partum women imposes any danger of occurring
PPT. Sixty hundred and ten pregnant women were involved in the cohort just before
delivery. Four hundred and eighty-eight (80%) of them accepted taking part in
follow-ups more than 6 months post-partum. A blood sample was taken from
participants before delivery and every 3 months post-partum for testing of serum
TSH, thyroid autoantibodies. Free T3 (FT3), free T4 (FT4) and TSH receptor
antibody (TRAb) were detected if TSH was abnormal. The iodine nutrition was
evaluated according to the mean level of the fasting urinary iodine excretions at
different times during the studying period, and participants were subgrouped into
3 categories with low, adequate and high iodine intake. For those participants
who had thyroid dysfunction within 6 months post-partum, the follow-up persisted
for 1 yr. Of 488 pregnant women, PPT developed in 11.9% (58/488). Given overt and
subclinical PPT, the prevalence was 7.17% (no.=35) and 4.71% (no.=23),
respectively. There was a strong association between the presence of thyroid
peroxidase antibody (TPOAb) at delivery and the risk of developing PPT [RR=6.76,
95% (CI) 4.42-10.34]. Overt cases had much higher titers of TPOAb than
subclinical patients (all p<0.05). The median urinary iodine (MUI) of patients
with PPT was significantly higher than that of healthy women (231.93 vs 199.88
microg/l p=0.00153). Both the prevalence of PPT and positive TPOAb rise with the
increment of iodine intakes. Pregnant women with high iodine intake had more risk
of developing PPT when compared with those with low iodine intake (RR=2.92, 95%CI
1.31-6.50). We concluded that positive TPOAb was of value for predicting the
occurrence and severity of PPT, and a high iodine intake was a risk factor
triggering PPT.

Thyroid. 2001 May;11(5):501-10.
Iodine-Induced hypothyroidism.
Markou K, Georgopoulos N, Kyriazopoulou V, Vagenakis AG.
Department of Medicine, University of Patras Medical School, Greece.
Iodine is an essential element for thyroid hormone synthesis. The thyroid gland
has the capacity and holds the machinery to handle the iodine efficiently when
the availability of iodine becomes scarce, as well as when iodine is available in
excessive quantities. The latter situation is handled by the thyroid by acutely
inhibiting the organification of iodine, the so-called acute Wolff-Chaikoff
effect, by a mechanism not well understood 52 years after the original
description. It is proposed that iodopeptide(s) are formed that temporarily
inhibit thyroid peroxidase (TPO) mRNA and protein synthesis and, therefore,
thyroglobulin iodinations. The Wolff-Chaikoff effect is an effective means of
rejecting the large quantities of iodide and therefore preventing the thyroid
from synthesizing large quantities of thyroid hormones. The acute Wolff-Chaikoff
effect lasts for few a days and then, through the so-called "escape" phenomenon,
the organification of intrathyroidal iodide resumes and the normal synthesis of
thyroxine (T4) and triiodothyronine (T3) returns. This is achieved by decreasing
the intrathyroidal inorganic iodine concentration by down regulation of the
sodium iodine symporter (NIS) and therefore permits the TPO-H202 system to resume
normal activity. However, in a few apparently normal individuals, in newborns and
fetuses, in some patients with chronic systemic diseases, euthyroid patients with
autoimmune thyroiditis, and Graves' disease patients previously treated with
radioimmunoassay (RAI), surgery or antithyroid drugs, the escape from the
inhibitory effect of large doses of iodides is not achieved and clinical or
subclinical hypothyroidism ensues. Iodide-induced hypothyroidism has also been
observed in patients with a history of postpartum thyroiditis, in euthyroid
patients after a previous episode of subacute thyroiditis, and in patients
treated with recombinant interferon-alpha who developed transient thyroid
dysfunction during interferon-a treatment. The hypothyroidism is transient and
thyroid function returns to normal in 2 to 3 weeks after iodide withdrawal, but
transient T4 replacement therapy may be required in some patients. The patients
who develop transient iodine-induced hypothyroidism must be followed long term
thereafter because many will develop permanent primary hypothyroidism.

Hokkaido Igaku Zasshi 1994 May;69(3):614-26.
[Screening for thyroid dysfunction in adults residing in Hokkaido Japan: in
relation to urinary iodide concentration and thyroid autoantibodies]
[Article in Japanese]
Konno N, Iizuka N, Kawasaki K, Taguchi H, Miura K, Taguchi S, Murakami S,
Hagiwara K, Noda Y, Ukawa S.
Department of Internal Medicine, Hokkaido Central Hospital for Social Health
Insurance, Sapporo, Japan.
The prevalence of thyroid dysfunction and its relation to thyroid autoantibodies
(TAA) and urinary iodide concentration (UI) was studied in apparently healthy
adults in Sapporo (n = 4110) (Sapporo group), and in five coastal areas of
Hokkaido (n = 1061) (coastal group) which produce iodine-rich seaweed (kelp).
The frequency of above normal UI (high UI) in the morning urinary samples of
coastal group was 10.8%, significantly higher than that of Sapporo group (6.4%)
(p < 0.001). Frequency of positive TAA in both groups were similar. In Sapporo
group TAA was positive in 6.4% of males and 13.8% of females with an age-related
increase. The overall prevalence of hyperthyroidism (TSH < 0.15 mU/L) in coastal
group (0.6%) was similar to that in Sapporo group (1.1%), while that of
hypothyroidism (TSH > 5.0 mU/L) in coastal group (3.8%) was significantly higher
than that in Sapporo group (1.3%) (P < 0.001). The frequency of high UI
correlated significantly with that of hypothyroidism with negative TAA (r =
0.829, P < 0.05), but not with positive TAA, or with that of hyperthyroidism.
Hypothyroidism was more prevalent in TAA negative subjects with high UI than
with normal UI. Moreover, serum TSH and thyroglobulin levels were higher and
free T4 level was lower in former than in latter group. These results indicate
that 1) the prevalence of TAA negative hypothyroidism in iodine sufficient areas
may be associated with the amount of iodine ingested, 2) this hypothyroidism is
more prevalent and marked in subjects consuming further excess amounts of
iodine, and 3) excessive intake of iodine should be considered an etiology of
hypothyroidism in addition to chronic thyroiditis in these areas.

Clin Endocrinol (Oxf) 1989 Oct;31(4):453-65
Thyroid autoimmunity in endemic goitre caused by excessive iodine intake.
Boyages SC, Bloot AM, Maberly GF, Eastman CJ, Li M, Qian QD, Liu DR, van der
Gaag RD, Drexhage HA.
Department of Medicine, Westmead Hospital, Sydney, Australia.
The pathophysiology of endemic goitre caused by excessive iodine intake is not
well defined. By interacting with the immune system, iodine excess may trigger
the development of autoimmune thyroid disease such as lymphocytic Hashimoto's
thyroiditis (LT). In an attempt to examine this further, we compared the
presence of thyroid autoantibodies in 29 goitrous children, from an iodine
excess area, and in 26 healthy children, from an iodine sufficient area, of
north central China. Serum was tested for antimicrosomal (MAb),
anti-thyroglobulin (TgAb), second colloid antigen antibodies (CA2-Ab) and TSH
binding inhibitory immunoglobulins (TBII). Affinity chromatographically purified
IgG was tested for thyroid growth-stimulating activity (TGI) by two different
methods: a sensitive cytochemical bioassay (CBA) using guinea-pig thyroid
explants and a mitotic arrest assay (MAA) employing a continuous rat thyroid
cell line (FRTL-5). We found no increased prevalence of LT in patients with
endemic iodine goitre. The levels of MAb, TgAb and CA2-Ab did not differ
significantly between the two groups of children. Further, TBII were not present
in either group. Thyroid growth-stimulating immunoglobulins (TGI) were the major
autoantibodies found in children with goitres caused by iodine excess. In the
CBA, 12 of 20 (60%) goitrous children and 0 of 12 (0% P less than 0.05) healthy
children were positive for TGI. Similar results were found in the MAA, and a
good correlation between results of the CBA and MAA was found (P = 0.003).
Maximal TGI activity in dose-response CBA showed a good relation with clinical
goitre size (r = 0.63; P less than 0.05) indicating a possible
pathophysiological role for these antibodies. We conclude that endemic iodine
goitre is not associated with Hashimoto's lymphocytic thyroiditis. Nevertheless,
autoimmune growth factors such as TGI may play a primary role in the
pathogenesis of thyroid growth in this condition.

Am J Clin Nutr. 2005 Apr;81(4):840-4.
High thyroid volume in children with excess dietary iodine intakes.
Zimmermann MB, Ito Y, Hess SY, Fujieda K, Molinari L.
Human Nutrition Laboratory, Swiss Federal Institute of Technology, Zurich,
Switzerland. [email protected]
BACKGROUND: There are few data on the adverse effects of chronic exposure to
high iodine intakes, particularly in children. OBJECTIVE: The objective of the
study was to ascertain whether high dietary intakes of iodine in children result
in high thyroid volume (Tvol), a high risk of goiter, or both. DESIGN: In an
international sample of 6-12-y-old children (n = 3319) from 5 continents with
iodine intakes ranging from adequate to excessive, Tvol was measured by
ultrasound, and the urinary iodine (UI) concentration was measured. Regressions
were done on Tvol and goiter including age, body surface area, sex, and UI
concentration as covariates. RESULTS: The median UI concentration ranged from
115 microg/L in central Switzerland to 728 microg/L in coastal Hokkaido, Japan.
In the entire sample, 31% of children had UI concentrations >300 microg/L, and
11% had UI concentrations >500 microg/L; in coastal Hokkaido, 59% had UI
concentrations >500 microg/L, and 39% had UI concentrations >1000 microg/L. In
coastal Hokkaido, the mean age- and body surface area-adjusted Tvol was
approximately 2-fold the mean Tvol from the other sites combined (P < 0.0001),
and there was a positive correlation between log(UI concentration) and log(Tvol)
(r = 0.24, P < 0.0001). In the combined sample, after adjustment for age, sex,
and body surface area, log(Tvol) began to rise at a log(UI concentration) >2.7,
which, when transformed back to the linear scale, corresponded to a UI
concentration of approximately 500 microg/L. CONCLUSIONS: Chronic iodine intakes
approximately twice those recommended-indicated by UI concentrations in the
range of 300-500 microg/L-do not increase Tvol in children. However, UI
concentrations >/=500 microg/L are associated with increasing Tvol, which
reflects the adverse effects of chronic iodine excess.
Multicenter Study

Acta Endocrinol (Copenh) 1978 Aug;88(4):703-12
A case of Hashimoto's thyroiditis with thyroid immunological abnormality
manifested after habitual ingestion of seaweed.
Okamura K, Inoue K, Omae T.
An interesting case of iodide induced goitre with immunological abnormalities is
described. The patient who was sensitive to synthetic penicillin had previously
been treated for exudative pleuritis, congestive heart failure and acute renal
failure. Following recovery, he began to ingest large amounts of seaweed after
which he developed goitrous hypothyroidism. It was of interest that the serum
level of gamma-globulin increased, and subsequently the antithyroid microsomal
antibody became strongly positive, suggesting that thyroidal autoimmune
processes had been precipitated. Biopsy of the thyroid gland revealed chronic
thyroiditis, with evidence suggesting extreme stimulation by TSH. Hight
thyroidal uptake of 131I, positive perchlorate discharge test and biochemical
analysis of the thyroidal soluble protein showed severe impairment of hormone
synthesis following continuous accumulation of excess iodide. While there is
evidence suggesting that increased iodide may be an important factor in the
initiation of Hashimoto's thyroiditis, this may result from the marked increased
sensitivity of Hashimoto's gland to the effects of iodine. Thus an occult lesion
could be unmasked in this manner. The mechanism by which iodide mediates this
effect is not clear.

Presse Med 2002 Oct 26;31(35):1670-5
[Hypothyroidism related to excess iodine]
[Article in French]
Wemeau JL.
Clinique endocrinologique Marc Linquette CHRU de Lille USNA, 59037 Lille.
[email protected]
WOLFF-CHAIKOFF'S EFFECT: The thyroid gland has a capacity to reduce thyroid
hormone production in the presence of excess iodine by reducing the
organification of the iodine. This Wolff-Chaikoff effect is observed after 48
hours and protects the organism from excessive synthesis of the thyroid
hormones. This effect is usually temporary and within a few days thyroid hormone
synthesis returns to normal through the so-called 'escape' phenomenon. However
in a few normal individuals and in some susceptible patients, the escape does
not occur. THE CONTEXT OF OCCURRENCE: Iodine-induced hypothyroidism is observed
in fetuses, newborn, adults and in the elderly. It is observed in individuals
without underlying overt thyroid disorder, and specially in patients with
autoimmune thyroiditis or those previously treated for thyroid diseases (Graves'
disease, subacute or pospartum thyroiditis, iatrogenic thyroid dysfunction...).
FROM A CLINICAL AND PROGRESSIVE POINT OF VIEW: The hormone deficiency is of
obvious clinical expression, or sometimes discreet and revealed by hormone
exploration. It is usually temporary, regressing with a few days or weeks after
iodine withdrawal. Nevertheless, some patients require transient hormone
replacement therapy.

Bull Mem Acad R Med Belg 1989;144(5-7):313-8; discussion 318-20
[Experimental goiter formation]
[Article in French]
Denef JF.
Nodules formation in goiter is still poorly understood due to the lack of an
adequate animal model. The key role of iodine in the increased heterogeneity of
iodine metabolism and in cold follicle formation has been demonstrated.
Administration of iodide excess to goitrous mice induces follicle cell necrosis
and thyroiditis. Necrosis and inflammation can be prevented by reducing the
iodine dose, giving T3 or T4, or combining iodide with antithyroid drugs or
vitamin E. This suggest that iodide toxicity is related to excessive production
of free radicals. During inflammation, Ia positive interstitial cells were
increased in number whereas no Ia expression was seen in follicular cells.

Clin Endocrinol (Oxf) 1989 Oct;31(4):453-65
Thyroid autoimmunity in endemic goitre caused by excessive iodine intake.
Boyages SC, Bloot AM, Maberly GF, Eastman CJ, Li M, Qian QD, Liu DR, van der
Gaag RD, Drexhage HA.
Department of Medicine, Westmead Hospital, Sydney, Australia.
The pathophysiology of endemic goitre caused by excessive iodine intake is not
well defined. By interacting with the immune system, iodine excess may trigger
the development of autoimmune thyroid disease such as lymphocytic Hashimoto's
thyroiditis (LT). In an attempt to examine this further, we compared the
presence of thyroid autoantibodies in 29 goitrous children, from an iodine
excess area, and in 26 healthy children, from an iodine sufficient area, of
north central China. Serum was tested for antimicrosomal (MAb),
anti-thyroglobulin (TgAb), second colloid antigen antibodies (CA2-Ab) and TSH
binding inhibitory immunoglobulins (TBII). Affinity chromatographically purified
IgG was tested for thyroid growth-stimulating activity (TGI) by two different
methods: a sensitive cytochemical bioassay (CBA) using guinea-pig thyroid
explants and a mitotic arrest assay (MAA) employing a continuous rat thyroid
cell line (FRTL-5). We found no increased prevalence of LT in patients with
endemic iodine goitre. The levels of MAb, TgAb and CA2-Ab did not differ
significantly between the two groups of children. Further, TBII were not present
in either group. Thyroid growth-stimulating immunoglobulins (TGI) were the major
autoantibodies found in children with goitres caused by iodine excess. In the
CBA, 12 of 20 (60%) goitrous children and 0 of 12 (0% P less than 0.05) healthy
children were positive for TGI. Similar results were found in the MAA, and a
good correlation between results of the CBA and MAA was found (P = 0.003).
Maximal TGI activity in dose-response CBA showed a good relation with clinical
goitre size (r = 0.63; P less than 0.05) indicating a possible pathophysiological role
for these antibodies. We conclude that endemic iodine goitre is not associated with
Hashimoto's lymphocytic thyroiditis. Nevertheless, autoimmune growth factors such as
TGI may play a primary role in the pathogenesis of thyroid growth in this condition.

J Am Diet Assoc 1990 Nov;90(11):1571-81
A review of iodine toxicity reports.
Pennington JA.
Division of Nutrition, Food and Drug Administration, Washington, DC 20204.
This article summarizes case reports, population studies, and experimental
studies from the literature concerning adverse effects of exposure to iodine
from the mid-1880s to 1988. Exposure to excessive iodine through foods, dietary
supplements, topical medications, and/or iodinated contrast media has resulted
in thyroiditis, goiter, hypothyroidism, hyperthyroidism, sensitivity reactions,
or acute responses for some individuals. Reports of maternal iodine exposure
during pregnancy or lactation affecting newborn or nursing infants are cited.
Susceptibility to excess iodine is discussed as well as the relationship between
dose and response. It is concluded that some individuals can tolerate very high
levels of iodine with no apparent side effects and that iodine intakes less than
or equal to 1.000 mg/day are probably safe for the majority of the population,
but may cause adverse effects in some individuals. Determination of maximum
tolerable levels of iodine intake will require human experimental studies at
levels between 0.150 and 1.000 mg/day for normal subjects, subjects with
autonomous thyroid tissue, and iodine-sensitive subjects.

Autoimmunity 1994;18(1):31-40
Iodide induced lymphocytic thyroiditis in the BB/W rat: evidence of direct toxic
effects of iodide on thyroid subcellular structure.
Li M, Boyages SC.
Department of Clinical Endocrinology, Westmead Hospital, NSW, Australia.
A high dietary iodine intake accelerates the development of lymphocytic
thyroiditis (LT) in the BB/W rat. Our previous studies have defined the temporal
sequence of the immunological events triggered by excess iodide intake in these
animals. It was still not clear, however, whether these observed immunological
changes were a direct effect on immune effector cells, or whether they
represented a secondary response to a toxic effect of iodine on thyroid tissue.
In the present study, the effect of excessive iodine intake on the subcellular
structure of the BB/W rat thyroid gland, particularly, whether iodide had a
toxic effect independent of its immune response has been examined. BB/W rats
were exposed, prenatally through maternal drinking water, to excessive iodide at
two doses (Moderate 3 x 10(-6) M iodide/l; High 3 x 10(-3) M iodide/l); a third
group of BB/W rats was given tap water; till 12 weeks postnatal age. Two groups
of Wistar rats received high dose iodide water or tap water for the same period
of time and served as controls. Thyroid gland ultrastructure was determined by
electron microscopic (EM) examination. Thyroid 125I uptake and perchlorate
discharge tests were also performed in separate experiments. We found that
thyroid glands of non-iodine supplemented Wistar rats were morphlogically normal
under EM. There were no overt changes in the iodide treated Wistar rats. By
contrast, iodide treated BB/W rats exhibited marked accumulation of secondary
lysosomes and lipid droplets; markedly swollen and disrupted mitochondria and
extreme dilatation of rough endoplasmic reticulum (RER).

Clin Immunol Immunopathol 1993 Nov;69(2):189-98
An excess of dietary iodine accelerates the development of a thyroid-associated
lymphoid tissue in autoimmune prone BB rats.
Mooij P, de Wit HJ, Drexhage HA.
Department of Immunology, Erasmus University, Rotterdam, The Netherlands.
Previous studies have shown that dietary iodine enhances the severity and
incidence of focal thyroiditis in autoimmune BB rats and OS chickens. However,
which lymphoid cells are involved in the development of the iodine-induced focal
thyroiditis and what the consequences are for the anticolloid antibody
production have not been studied in detail. We therefore performed a study in
which 3-week-old female BB rats were kept on either an enriched iodine diet
(EID; iodine intake, 100 micrograms iodine/day) or a normal iodine diet (NID;
iodine intake, 7 micrograms iodine/day) for a period of 18 weeks. The
development of the focal thyroiditis was immunohistologically studied.
Immunohistological data were compared to the thyroid hormone status and
anti-colloid antibody production. Our data confirm that a high dietary iodine
intake results in an accelerated development of the focal lymphoid cell
infiltrates in the thyroid of the BB rat. After 12-18 weeks of an EID 50% of the
BB rats developed these infiltrates. Our data additionally show that: (a) the
process starts with increases in the number of infiltrating MHC class
II-positive dendritic cells and a clustering of these cells with T cells, B
cells, and some macrophages and (b) the focal infiltrates are highly organized
and consist of central B cell follicle-like structures surrounded by rims and
areas of T cells. The architecture of the focal thyroiditis is hence very
similar to mucosa-associated lymphoid tissue and secondary lymphoid organs
(spleen and lymph node). Only minor signs of thyrocyte destruction were
observed. We therefore consider the term "thyroiditis" as inappropriate and
prefer the term "thyroid-associated lymphoid tissue." Since the thyroiditis
component was small, it is also not surprising that the BB rats on the EID
remained euthyroid. The presence of the thyroid-associated lymphoid tissue in
the BB rats was positively correlated to the presence of anti-colloid antibody
in the serum of the BB rats. We speculate that the dietary iodine might have
direct effects on cells of the immune system or on cells forming the
microenvironment of lymphoid tissue (reticulum cells). A role for highly
iodinated thyroglobulin in the accelerated development of thyroid-associated
lymphoid tissue is also possible.

Endocrinology 1987 Aug;121(2):481-5
Iodine-induced thyroiditis and hypothyroidism in the hemithyroidectomized BB/W
rat.
Allen EM, Appel MC, Braverman LE.
We have recently reported that iodine administration (0.05% iodine in drinking
water) to weanling, diabetes mellitus- and lymphocytic thyroiditis (LT)-prone
Biobreeding Worcester (BB/W) rats strikingly increases the incidence of LT
without occurrence of iodine-induced hypothyroidism, which frequently results
when excess iodine is administered to euthyroid patients with Hashimoto's
thyroiditis. Since hypothyroidism did not occur in the iodine-treated BB/W rats,
hemithyroidectomy was carried out in 30-day-old BB/W rats to increase thyroid
mass and functional reserve. Iodine administration for 60 days markedly
increased antithyroglobulin antibodies (0.40 +/- 0.08 vs. 0.15 +/- 0.06 OD; P
less than 0.02), the incidence of LT (68% vs. 13%; P less than 0.001), and
thyroid weight of the residual lobe (10.5 +/- 0.7 vs. 6.3 +/- 0.3 mg/100 g BW; P
less than 0.001) and induced hypothyroidism (T4, 2.5 +/- 0.2 vs. 3.0
micrograms/dL; P less than 0.05; T3, 25.1 +/- 1.9 vs. 37.5 ng/dL; P less than
0.001; TSH, 252 +/- 49 vs. 61 +/- 14 microU/mL; P less than 0.02).
Hypothyroidism in the iodine-treated rats occurred primarily in those with LT.
Similar studies were carried out in the non-diabetes mellitus-, non-LT-prone,
genetically equivalent BB/W rats (W-line), the parent strain Wistar-Furth rats,
and Sprague-Dawley rats. Iodine administration did not induce LT or
antithyroglobulin antibodies in these three strains and did not affect thyroid
function in Wistar-Furth and Sprague-Dawley rats. However, in the W-line rats,
iodine excess did induce thyroid enlargement in the residual lobe (8.4 +/- 0.2
vs. 6.4 +/- 0.2 mg/100 g BW; P less than 0.001), a decrease in serum T3 (71.5
+/- 2.9 vs. 86.0 +/- 2.5 ng/dL; P less than 0.001), and an increase in serum TSH
(344 +/- 65 vs. 69 +/- 6.0 microU/mL; P less than 0.001). It is evident,
therefore, that hemithyroidectomy in BB/W rats sufficiently reduces functioning
thyroid tissue, resulting in iodine-induced LT and hypothyroidism, similar to
iodine-induced hypothyroidism in euthyroid patients with Hashimoto's
thyroiditis. It is unclear, however, why iodine administration also induced
hypothyroidism in hemithyroidectomized, genetically similar, W-line rats in the
absence of LT. This observation suggests that iodine-induced hypothyroidism in
rats may be genetically determined.

Exp Mol Pathol 1986 Jun;44(3):259-71
Direct toxic effect of iodide in excess on iodine-deficient thyroid glands:
epithelial necrosis and inflammation associated with lipofuscin accumulation.
Mahmoud I, Colin I, Many MC, Denef JF.
Involution of thyroid hyperplasia (induced by a low iodine diet and a goitrogen,
propylthiouracil, PTU) was obtained in mice by administering a high or a
moderate dose of iodide (HID or MID, respectively). In HID involuting glands,
vasoconstriction was observed after 12 hr whereas necrosis and inflammation were
very abundant as early as after 6 hr and maximal after 48 hr. They were not
prevented by papaverine by which vasoconstriction was inhibited, but were
inhibited by the continuation of PTU by which iodide oxidation and
organification were inhibited. Lipofuscin inclusions in thyroid and inflammatory
cells were always associated with necrosis. On the contrary, when involution was
induced by MID or by HID + triiodothyronine (T3), or by T3 alone, neither
necrosis nor inflammation occurred and apoptosis was the only mode of cell
deletion. No lipofuscin inclusion occurred. Our results demonstrate that iodide
in excess, after being oxidized or organified, is directly toxic for
iodine-deficient thyroid cells. The presence of lipofuscin suggests that its
toxicity is mediated by lipid peroxidation, a consequence of production of free
radicals in excess.

J Clin Invest 1991 Jul;88(1):106-11
Uptake and metabolism of iodine is crucial for the development of thyroiditis in
obese strain chickens.
Brown TR, Sundick RS, Dhar A, Sheth D, Bagchi N.
Department of Medicine, Immunology and Microbiology, Wayne State University,
Detroit, Michigan 48201.
To assess the importance of the role of thyroidal iodine in the pathogenesis of
thyroiditis in the obese strain (OS) chicken, a model of spontaneous and severe
disease, we studied the effect of antithyroid drugs that reduce thyroidal iodine
or prevent its metabolism. Reduction of thyroidal iodine was achieved with
KClO4, an inhibitor of iodine transport and mononitrotyrosine (MNT), a drug that
promotes loss of thyroidal iodine as iodotyrosines. A regimen consisting of
KClO4 and MNT administration beginning in ovo and continuing after hatching
reduced thyroidal infiltration to 2% of control values and decreased
thyroglobulin antibody (TgAb) production for as long as 9 wk. Untreated birds
had severe disease by 5 wk of age. The suppression of disease was independent of
TSH, not mediated by generalized immunosuppression and reversed by excess
dietary iodine. Two drugs that inhibit the metabolism of iodine,
propylthiouracil (PTU) and aminotriazole, reduced thyroidal infiltration and
TgAb levels, although to a lesser extent. When splenocytes from OS chickens with
thyroiditis were transferred to Cornell strain (CS) chickens, a related strain
that develops late onset mild disease, only the recipients that were iodine
supplemented developed thyroiditis. In conclusion, autoimmune thyroiditis in an
animal model can be prevented by reducing thyroidal iodine or its metabolism and
optimal effects require intervention at the embryonic stage.

Autoimmunity 1993;14(3):181-7
Iodine induced lymphocytic thyroiditis in the BB/W rat: early and late immune
phenomena.
Li M, Eastman CJ, Boyages SC.
Department of Clinical Endocrinology, Westmead Hospital, NSW, Australia.
The effect of iodine excess on thyroid function and on the immunological
sequence of events leading to lymphocytic thyroiditis (LT) was studied in the NB
subline of BB/W rats to determine the mechanisms by which the level of iodine
intake influences the development of LT in this animal model. Iodine
supplemented water (500 micrograms/l, Group 1 or 500 mg/l, Group 2) or
non-iodine supplemented tap water (Group 3) was given to breeding pairs and
their offspring ad libitum. A Wistar rat group, also given tap water (Group 4)
served as controls. To determine the immunological sequence of events, the
phenotypic nature of the infiltrating thyroid lymphocytes was examined by
specific immunoperoxidase staining in BB/W and Wistar rats at 6, 9, 12, and 15
weeks. Antigen-presenting cells and class II (Ia) antigen expression on
thyrocytes were also examined. The first immunological event apparent in the
iodine-treated BB/W rats was a sharp increase in the number of Ia positive
dendritic cells at 9 weeks compared with control BB/W and Wistar rats. In the
iodine excess groups dendritic cells were associated with scattered areas of
lymphocytic infiltration, comprising predominantly T helper cells (W3/25). T
suppressor cells (OX 8) and IL-2 receptor positive activated T-cells (OX 39)
were both present in small numbers. B-cells (OX 12) were absent. In addition,
thyrocytes did not exhibit Ia antigen expression. By contrast, lymphocytic
infiltration was not found at 9 weeks in control BB/W rats.(ABSTRACT TRUNCATED
AT 250 WORDS)

J Clin Endocrinol Metab 1992 Nov;75(5):1273-7
Iodine-induced subclinical hypothyroidism in euthyroid subjects with a previous
episode of amiodarone-induced thyrotoxicosis.
Roti E, Minelli R, Gardini E, Bianconi L, Gavaruzzi G, Ugolotti G, Neri TM,
Braverman LE.
Centro per lo Studio, Prevenzione, Diagnosi e Cura delle Tireopatie, Universita
di Parma, Italy.
Amiodarone-induced thyrotoxicosis (AIT) occurs most frequently in patients with
underlying thyroid disease and is generally believed to be due to the iodine
contamination of amiodarone and iodine released by the metabolism of the drug.
We and others have suggested that the thyrotoxicosis may also be secondary to
amiodarone-induced thyroiditis. To further determine the etiology of AIT, we
administered large doses of iodides [10 drops saturated solution of potassium
iodide (SSKI) daily] to 10 euthyroid patients long after an episode of AIT
believed to be due at least in part to amiodarone-induced thyroiditis. Six of
these 10 patients had an abnormal iodide-perchlorate discharge test before SSKI
administration, indicating a subtle defect in the thyroidal organification of
iodide. During SSKI administration, 6 patients developed marked iodine-induced
basal and/or TRH-stimulated serum TSH elevations, 2 had suppressed basal and
TRH-stimulated TSH values, and 2 had normal TSH responses compared to
SSKI-treated euthyroid subjects with no history of amiodarone ingestion or
thyroid disease. Serum T4 and T3 concentrations remained normal and unchanged
during SSKI administration in both the AIT patients and control subjects. These
results strongly suggest that excess iodine may not be the cause of the
hyperthyroidism associated with amiodarone therapy, especially in those patients
with probable amiodarone-induced thyroiditis. Furthermore, like patients with a
previous history of subacute thyroiditis and postpartum thyroiditis, the present
results suggest that some patients with a previous history of AIT may be at risk
to develop hypothyroidism when given excess iodine.

Endokrynol Pol 1992;43 Suppl 1:53-69
The relationship between autoimmune thyroid disease and iodine intake: a review.
Foley TP Jr.
Division of Endocrinology, Metabolism and Diabetes Mellitus, School of Medicine,
University of Pittsburgh.
There is evidence to suggest that elevated levels of iodide in the diet are
associated with autoimmune thyroid disease (ATD) in susceptible individuals, and
that autoimmune thyroiditis (Hashimoto's disease) is less common in susceptible
individuals who live in regions with dietary iodine deficiency. There are
epidemiologic studies in endemic goiter areas that report an increase in ATD,
particularly thyroiditis, after the therapeutic administration of iodized salt,
bread and oil. Lymphocytic infiltration of the thyroid is rarely found in
patients from severe endemic goiter regions, yet there is a reversal of this
observation after dietary iodine supplementation. Thyroid antibodies, both
thyroglobulin (TgAb) and peroxidase (TpAb) or microsomal, were not detected in
serum from patients with endemic goiter, but became positive in 43% of subjects
three and six months after therapy with iodized oil, and there developed
transient hyperthyroidism. Similarly, the addition of iodine to the diet or the
administration of iodine-containing medications increases the frequency of ATD
and the severity of existing autoimmune thyroiditis. Furthermore, autoimmune
thyroiditis has been induced by the administration of excess iodide to strains
of chickens and rats that are genetically predetermined to develop the disease.
We are beginning to understand the pathogenesis of ATD. In hyperthyroidism the
evidence clearly supports the hypothesis that TSH receptor antibodies (TRAb)
stimulate the TSH receptor to induce excessive and sustained secretion of
thyroid hormones. Cellmediated immune mechanisms, such as antibody dependent
cellmediated cytotoxicity (ADCC), initiate the lymphocytic infiltration and
thyrocytotoxicity in autoimmune thyroiditis. The mechanisms that initiate the
development of the abnormal immune response and the relationship of ATD with
excess iodide are poorly understood. There is evidence that an increase in the
iodination of thyroglobulin (Tg) enhances its immunogenicity. The results of
clinical and experimental studies support the requirement of a genetic
predisposition to the development of ATD that may be precipitated by exposure to
certain environmental factors. Another mechanism supported by experimental data
is the direct toxic effect of excess iodide on iodide-deficient thyroid glands.
High concentrations of iodide after oxidation to iodine causes epithelial
necrosis and inflammation associated with lipofuscin accumulation suggestive of
toxicity mediated by lipid peroxidation from excessive amounts of free radicals.
The epithelial damage would initiate inflammatory and immune responses. Although
these mechanisms would relate to the onset of autoimmune thyroiditis on exposure
to excessive amounts of iodide, the relationship of iodide intake and autoimmune
hyperthyroidism is less clear.(ABSTRACT TRUNCATED AT 400 WORDS)

Clin Immunol Immunopathol 1996 Dec;81(3):287-92
Iodine-induced autoimmune thyroiditis in NOD-H-2h4 mice.
Rasooly L, Burek CL, Rose NR.
Department of Molecular Microbiology and Immunology, School of Hygiene and
Public Health, Johns Hopkins University, Baltimore, Maryland 21205, USA.
Excess iodine ingestion has been implicated in induction and exacerbation of
autoimmune thyroiditis in human populations and animal models. We studied the
time course and sex-related differences in iodine-induced autoimmune thyroiditis
in NOD-H-2h4 mice. This strain, derived from a cross of NOD with B10.A(4R),
spontaneously develops autoimmune thyroiditis but not diabetes. NOD-H-2h4 mice
were given either plain water or water with 0.05% iodine for 8 weeks.
Approximately 54% of female and 70% of male iodine-treated mice developed
thyroid lesions, whereas only 1 of 20 control animals had thyroiditis at this
time. Levels of serum thyroxin (T4) were similar in the treatment and control
groups. Thyroglobulin-specific antibodies were present in the iodine-treated
group after 8 weeks of treatment but antibodies to thyroid peroxidase were not
apparent in the serum of any of the animals. Levels of thyroglobulin antibodies
increased throughout the 8-week iodine ingestion period; however, no correlation
was seen between the levels of total thyroglobulin antibodies and the degree of
thyroid infiltration at the time of autopsy. The thyroglobulin antibodies
consisted primarily of IgG2a, IgG2b, and IgM antibodies with no detectable IgA,
IgG1, or IgG3 thyroglobulin-specific antibodies. The presence of IgG2b
thyroglobulin-specific antibodies correlated well with the presence of thyroid
lesions.

Verh Dtsch Ges Pathol 1996;80:297-301
[Spontaneous Hashimoto-like thyroiditis in cats]
[Article in German]
Schumm-Draeger PM, Langer F, Caspar G, Rippegather K, Herrmann G, Fortmeyer HP,
Usadel KH, Hubner K.
Medizinische Klinik I, Johann Wolfgang Goethe-Universitat, Frankfurt/M.
A breeding line of domestic cats spontaneously developing symptoms of
hypothyroidism between the 40th and 60th day of life (fur changes, loss of
appetite, growth retardation), elevated levels of antibodies against microsomal
structures and thyroglobulin, and lymphocytic thyroid infiltration has been
recently established at our facility. Aim of our studies was to examine the
effect of high iodine ingestion or prophylactic thyroid hormone therapy on
functional and morphological characteristics of this Hashimoto-like thyroiditis
in cat. From birth to day 80 of life cats were treated with iodine (n = 9; 0.1
mg/l) or thyroxin (n = 13; 2.0 micrograms/ kg/d) respectively. Untreated animals
served as controls (n = 12). Cat-serum was tested for thyroid function (TT3,
TT4). After 8 weeks the thyroid tissue was submitted to routine histological
processing (H&E) and the inflammatory activity was scored. Additionally
immunohistological staining was performed for MIB-1, IgG, IgM and MHCII
expression. Both untreated hypothyroid (UHC) as well as iodine-treated (IC) cats
revealed a significantly higher degree of thyroid inflammation and higher tissue
levels of IgM as the thyroxin-substituted animals (TC). Epithelial proliferation
decreased significantly in the IC and TC groups as compared to the untreated
controls. No significant differences regarding IgG production and HLAII
expression were detectable. Early thyroid hormone therapy significantly
decreases both incidence and activity of autoimmune thyroiditis in cats as
measured by inflammatory infiltration, IgM production and epithelial
proliferation. Animals with excess iodide intake, however, show an aggravation
of the autoimmune inflammatory activity.

Autoimmunity 1995;20(3):201-6
Excess iodine induces the expression of thyroid solid cell nests in lymphocytic
thyroiditis-prone BB/W rats.
Zhu YP, Bilous M, Boyages SC.
Department of Clinical Endocrinology, Westmead Hospital, Sydney, Australia.
Previous epidemiological studies have suggested that lymphocytic thyroiditis
and/or an increased iodine intake may be risk factors for the development of
thyroid cancer. We previously reported that excess iodine accelerated the
development of thyroid lymphocytic infiltration (LI) in the autoimmune BB/W rat
model. We also found that excess iodine increased thyroid cell proliferation in
a disordered manner. The present study was designed to further explore these
observations and to address the question as to whether excess iodine under
certain conditions predisposes the thyroid gland to neoplasia. To test this
hypothesis, the lymphocytic thyroiditis-prone BB/W rat was exposed to excess
iodine in drinking water. Ten BB/W rats at 4 weeks of age were given iodine
water (NaI 0.05%) for 10 weeks, whilst another 10 BB/W rats were given tap water
and served as controls. Eighteen normal Wistar rats were also divided into
excess iodine and control groups, served as a comparison to the BB/W rats. We
found that an excess iodine intake accelerated the development of LI in the BB/W
rat. Severe LI was usually accompanied by prominent thyroid cell proliferation,
evident as numerous microfollicles and cell masses, not forming normal thyroid
follicles. Numerous lymphocytes and plasma cells often encroached on these areas
of increased cellular proliferation. The surprising feature, and a possible
indicator of activated thyroid cell proliferation, was the high incidence of
thyroid solid cell nest-like lesions (SCN) in the iodine treated BB/W
rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Endocrinol Metab Clin North Am 1987 Jun;16(2):327-42
Environmental factors affecting autoimmune thyroid disease.
Safran M, Paul TL, Roti E, Braverman LE.
Department of Medicine, University of Massachusetts Medical Center, Worcester.
A number of environmental factors affect the incidence and progression of
autoimmune thyroid disease. Exposure to excess iodine, certain drugs, infectious
agents and pollutants, and stress have all been implicated.

Science 1985 Oct 18;230(4723):325-7
Induction of autoimmune thyroiditis in chickens by dietary iodine.
Bagchi N, Brown TR, Urdanivia E, Sundick RS.
Clinical studies have suggested that excess dietary iodine promotes autoimmune
thyroiditis; however, the lack of a suitable animal model has hampered
investigation of the phenomenon. In this study, different amounts of potassium
iodide were added to the diets of chicken strains known to be genetically
susceptible to autoimmune thyroiditis. Administration of iodine during the first
10 weeks of life increased the incidence of the disease, as determined by
histology and the measurement of autoantibodies to triiodothyronine, thyroxine,
and thyroglobulin. Further support for the relation between iodine and
autoimmune thyroiditis was provided by an experiment in which iodine-deficient
regimens decreased the incidence of thyroid autoantibodies in a highly
susceptible strain. These results suggest that excessive consumption of iodine
in the United States may be responsible for the increased incidence of
autoimmune thyroiditis.

Acta Endocrinol (Copenh) 1978 Aug;88(4):703-12
A case of Hashimoto's thyroiditis with thyroid immunological abnormality
manifested after habitual ingestion of seaweed.
Okamura K, Inoue K, Omae T.
An interesting case of iodide induced goitre with immunological abnormalities is
described. The patient who was sensitive to synthetic penicillin had previously
been treated for exudative pleuritis, congestive heart failure and acute renal
failure. Following recovery, he began to ingest large amounts of seaweed after
which he developed goitrous hypothyroidism. It was of interest that the serum
level of gamma-globulin increased, and subsequently the antithyroid microsomal
antibody became strongly positive, suggesting that thyroidal autoimmune
processes had been precipitated. Biopsy of the thyroid gland revealed chronic
thyroiditis, with evidence suggesting extreme stimulation by TSH. Hight
thyroidal uptake of 131I, positive perchlorate discharge test and biochemical
analysis of the thyroidal soluble protein showed severe impairment of hormone
synthesis following continuous accumulation of excess iodide. While there is
evidence suggesting that increased iodide may be an important factor in the
initiation of Hashimoto's thyroiditis, this may result from the marked increased
sensitivity of Hashimoto's gland to the effects of iodine. Thus an occult lesion
could be unmasked in this manner. The mechanism by which iodide mediates this
effect is not clear.

Presse Med 2002 Oct 26;31(35):1670-5
[Hypothyroidism related to excess iodine]
[Article in French]
Wemeau JL.
Clinique endocrinologique Marc Linquette CHRU de Lille USNA, 59037 Lille.
[email protected]
WOLFF-CHAIKOFF'S EFFECT: The thyroid gland has a capacity to reduce thyroid
hormone production in the presence of excess iodine by reducing the
organification of the iodine. This Wolff-Chaikoff effect is observed after 48
hours and protects the organism from excessive synthesis of the thyroid
hormones. This effect is usually temporary and within a few days thyroid hormone
synthesis returns to normal through the so-called 'escape' phenomenon. However
in a few normal individuals and in some susceptible patients, the escape does
not occur. THE CONTEXT OF OCCURRENCE: Iodine-induced hypothyroidism is observed
in fetuses, newborn, adults and in the elderly. It is observed in individuals
without underlying overt thyroid disorder, and specially in patients with
autoimmune thyroiditis or those previously treated for thyroid diseases (Graves'
disease, subacute or pospartum thyroiditis, iatrogenic thyroid dysfunction...).
FROM A CLINICAL AND PROGRESSIVE POINT OF VIEW: The hormone deficiency is of
obvious clinical expression, or sometimes discreet and revealed by hormone
exploration. It is usually temporary, regressing with a few days or weeks after
iodine withdrawal. Nevertheless, some patients require transient hormone
replacement therapy.

Thyroid 2001 May;11(5):427-36
Iodine and thyroid autoimmune disease in animal models.
Ruwhof C, Drexhage HA.
Department of Immunology, Erasmus University, Rotterdam.
Thyroid autoimmune diseases are complex, polygenic afflictions the penetrance of
which is heavily dependent on various environmental influences. In their
pathogenesis, an afferent stage (enhanced autoantigen presentation), a central
stage (excessive expansion and maturation of autoreactive T and B cells), and an
efferent stage (effects of autoreactive T cells and B cells on their targets)
can be discerned. At each stage, a plethora of inborn, endogenous or exogenous
factors is able to elicit the abnormalities characteristic of that stage, thus
opening the gateway to thyroid autoimmunity. Iodine is an important exogenous
modulating factor of the process. In general, iodine deficiency attenuates,
while iodine excess accelerates autoimmune thyroiditis in autoimmune prone
individuals. In nonautoimmune prone individuals, the effects of iodine are
different. Here iodine deficiency precipitates a mild (physiological) form of
thyroid autoimmune reactivity. Iodine excess stimulates thymus development.
Iodine probably exerts these effects via interference in the various stages of
the autoimmune process. In the afferent and efferent stage, iodine-induced
alterations in thyrocyte metabolism and even necrosis most likely play a role.
By contrast, in the central phase, iodine has direct effects on thymus
development, the development and function of various immune cells (T cells, B
cells macrophages and dendritic cells) and the antigenicity of thyroglobulin.

 

[windinthepines]

[2011]]

Me:
Hi Ray, Despite taking thyroid, and eating well, I still get winter
insomnia. I can't fall asleep until dawn, and then sleep during the
day. I talked to someone who fixed his similar insomnia issues with
1.25 mg of Bromocriptine a day. From what I read, it sounds to me like
Bromocriptine has a lot of negative side effects, and I couldn't find
any information on it curing insomnia. Aside from my insomnia, I still
often have diarrhea, and fatigue, which make me think that my problems
are related to serotonin. Do you think it might be worth trying
bromocriptine?

RP:

I have never tried it myself, but I know that some people have found it to be more effective than just thyroid. Some people have very intense reactions to it, flushing and low blood pressure for example, so it's good to be very cautious with it. I think it's best to work on thyroid and sugar metabolism, watching the temperature cycle and heart rate. What kind of thyroid product have you used?

Me:

When I started taking thyroid last year, I felt good taking a 1/4
Cynoplus and 12mcg Cynomel. With thyroid, I quickly gained 50 lbs, and
am no longer underweight. I felt more energetic, confident, and had a
positive outlook, and most of my eczema disappeared. I don't know what
happened, but something changed, and now I can't take any Cynoplus at
all without getting weird sensations in the back of my neck, and some
fingers--it feels like motor tics, or involuntary movements. So now
I'm taking 50mcg of Cynomel, broken up into 4mcg doses.

RP:

Is there enough sugar in your diet? Do you occasionally have seafood or liver, as a source of selenium?

Me: []

RP:

Something sugary (milk and honey, for example) right at bedtime might help with sleep.

Me:
I wrote to you before about taking bromocriptine for insomnia. In just
a few days, .6mg of bromocriptine seems to have mostly fixed my severe
insomnia. I don't like the feeling it gives me, so I'm not sure if
I'll continue to take it. I'm looking for other ways to get the same
effect. Do you think bromocriptine helped my sleep because of its
antiserotonin properties, or because it lowers prolactin? I was
thinking of trying Stablon instead, to see if it helps with my sleep
as well.

RP:

That's very interesting; I don't know what Stablon's effect might be, but a couple of people tell me they have had very good results from it.
I think winter-night stress involves all the hormones that regulate energy production, and getting lots of bright light on your face, head, and neck might help. A little niacinamide (100 mg), vitamins B1 and B6 (about 10 mg), and gelatin, sugar, and salt would help to maintain energy production during the dark.

 

[windinthepines]

[2011]

Me:
Hi Ray, I've been using many of your recommendations with great
success. If I eat your carrot salad, and avoid starches, my
long-standing digestion problems disappear. Recently I ate some bread
and beer, and have had a return of my symptoms. Usually I get small,
pulpy, yellowish feces that float, along with white fuzz on my tongue,
and a bad taste in my mouth. Does this sound like bacteria in my small
intestine

RP:

Yes, probably bacteria, maybe some yeast too. I have found that a pinch of flowers of sulfur, USP, can help to change the flora. About 80 years ago, doctors sometimes used camphoric acid; I tried it once, and had a perfectly clean tongue the next morning. Pregnenolone can help, too, but I'm not sure what the mechanism is. I used a daily carrot for years, and tried the other things when I got too tired of that. Bamboo shoots (boiled or canned) are a pleasant alternative to carrots.
Me:

Thanks. Pregnenolone seemed to help a little, although I feel spacey
and tired when I take it. I'll try flowers of sulfur when I get it. I
wonder if this bacteria/yeast problem is why I sometimes feel really
good on thyroid medicine and sometimes really bad. Right now I'm
taking 25mcg of Cynomel throughout the day, but I'm feeling fatigued
and depressed, with mostly normal bowel movements but also diarrhea
every other day or so, without really changing my foods.

RP:
I have found that aspirin helps with the bowel symptoms, and the associated fatigue/depression.

Me:
I've been noticing that my temperature is low when I wake up, but does
eventually get to 98.6 or higher. For instance, today it was 96.6 at
7am, and 97.0 at noon when I finally woke up, but later in the
afternoon it was 98.4. Should I pay attention to my temperature in the
morning more than at other times?

RP:
I think it's good for the whole curve to be a little higher. It should come up as your digestion improves, I think bacterial endotoxin interferes with energy production.

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

Me:
I read that it takes four years for the fat stores in our bodies to
change over. In your experience, do most people who switch to mostly
saturated dietary fats noticed that their metabolism increases slowly
over this four year period? I'm wondering if I can expect my health to
be better when the exchange is complete . I've been limiting PUFA for
two years, and while I sometimes feel very good, I often still feel
sluggish and unhealthy.

Thanks for your work,

RP:

Fat people with low metabolic rate probably take longer; when people
use a thyroid supplement they usually decrease it in the first couple
of years; it probably depends on age, too.

 

[windinthepines]

[2010]

Me:
Despite using bright lights, thyroid, pregnenolone, aspirin, caffeine, coconut oil, and a good diet, I'm getting sicker and more lethargic as the winter progresses here on the East Coast.

I've been reading about people who use LSD, psilocybin mushrooms, and various seeds to treat cluster headaches. Some people say that a single dose can sometimes prevent the recurrence of cluster headaches for months. Do you know if serotonin excess is the main problem with cluster headache sufferers? Does the long-term therapeutic value of these drugs come from 'resetting' serotonin excess?

Thanks

RP:
Have you seen any changes in your digestion?
(Intestinal inflammation is a major factor in
headaches and winter symptoms.) Are your
temperature and pulse rate optimal? Have you
checked for allergens among your foods or
supplements? People have told me that
bromocriptine and/or tianeptine (Stablon) helped
their headache, which would be consistent with a
serotonin problem. Does your diet include enough sugar?

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

Me:

[Gibberish]

RP:
Do you get enough selenium, for example from seafood? I usually use
roughly equal parts of T3 and T4, using small amounts of cynomel on
most days, occasionally cynoplus. Sometimes the intestinal flora can
interfere with the liver's hormone metabolism; raw carrots, milk,
bamboo shoots, and aspirin are things that often help with the flora
and liver function.

Me:

[Gibberish]

RP:

Experiments with brain slices showed that T4 competes against T3, causing an antimetabolic effect. Liver has all the nutrients, but it isn't ideal, because it also has antithyroid effects.

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

Me:

[Unimportant]

RP:
There are 25,000 unit capsules of retinyl palmitate, also of A from
halibut liver oil. I use them transdermally, because some of the
products have allergenic impurities, so I prefer the palmitate, that
doesn't smell like fish.

Me:
Can halogen bulbs provide helpful indoor light for northern winter months? If halogen bulbs give off more blue light, I was wondering if infrared bulbs might be better.

RP:
Regular incandescent bulbs, including those called infrared with
clear glass, are better, because of the low amount of blue.

======================
I wonder if your vitamin D might not be
deficient, as a result of reduced sun exposure.
Increased parathyroid hormone has many bad
effects, including insomnia. More milk and sugar
can help to compensate for low vitamin D, but
sunlight has other good effects. It takes the
body a few weeks to adjust to a given dose of
thyroid, so you should watch for changes in your temperature and pulse rate.


Me

[...]

RP:
I wonder if your vitamin D might not be
deficient, as a result of reduced sun exposure.
Increased parathyroid hormone has many bad
effects, including insomnia. More milk and sugar
can help to compensate for low vitamin D, but
sunlight has other good effects. It takes the
body a few weeks to adjust to a given dose of
thyroid, so you should watch for changes in your temperature and pulse rate.

Me:

[...]

RP:


The diarrhea would cause hypoglycemia with increased stress hormones and interference with thyroid function, so that would be the thing to figure out first, possibly trying grated carrot with a little salt, vinegar, and olive oil, in case there's a problem with the wrong kind of bacteria.

Me:

[...]

RP:

Yes, some people think their ideal ratio is two to one. The T3 action peaks in about an hour, and then fades gradually. Having some at intervals of a few hours allows you to adjust the dose according to how you feel, heart rate, sleep quality, etc.

 

[windinthepines]

[2013]

Me:

I enjoyed your last session on KMUD. I was thinking about the times and temperatures and pulses you talked about, and also about my typically inverted sleep pattern (sometimes 4am to 4pm). I could see this pattern as the result of high adrenalin and low thyroid, or high serotonin, estrogen, and histamine--the only other people I've talked to who sleep like this are women over 40, and I'm a younger man. What would you tell someone to do to reverse this? Set an alarm to take thyroid at regular waking hours?

RP:
Thyroid would be the basic thing, along with adjusting meals and light,
but it would probably be easiest to use some Benadryl or Periactin (and
aspirin, vitamin K) during the adjustment, for a few days to change a
couple of hours at a time.

Me:
Thanks. So I would want to wake up to take thyroid in the morning, when I want to be awake? What amount of aspirin might be helpful?


RP:
Thyroid helps to make sleep deeper, it doesn't help to wake up except by making sleep more restful. An aspirin an hour before bedtime can be helpful, but it should start gradually, with about 100 mg, gradually increasing in a few days to 500 mg.

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

Me:
I thought you might find this little anecdote from Gary Fisher interesting. In an interview I found on youtube, he was talking about his work with LSD in hospitals. He said that a doctor approached him, wanting to see if LSD might work as a pain drug for his dying cancer patients. The doctor apparently didn't really know what LSD was, and had no bad or good ideas about it.

One woman with cancer was given LSD. The next day she had no more pain. When she refused her regular pain medication, saying that she wasn't in pain and so didn't need medication, the cancer doctor got upset. He said that since the tests showed that she still had cancer, she must still be in pain. He concluded that the LSD had made her psychotic, and refused to test it on any more patients. Someone asked him if he'd rather have psychotic pain-free patients, or sane patients in pain, and he wanted the "sane" patients.

The doctor's attitude reminded me of what I've encountered, and heard others talk about. I was surprised that the attitude wasn't as new as I'd assumed, since I think this story is from the early '60s. Once I was pressured into seeing a doctor for my insomnia, and at the appointment he said that since insomnia and depression often appear together, I must be depressed, and needed to take an SSRI. One of my good friends has been in medical school for a few years, so I've had the opportunity to see how it's changed his thinking. I wonder if the most important components of this personality type are fear and compartmentalization--I learned about this from your writing, and from Altemeyer's book. Interestingly, Woody Allen has said that he's very good at compartmentalization, which helps him in making movies by avoiding distractions.

RP:

I had a friend whose experiences in Guatemala led to his taking science
courses at the U. of Oregon (where I met him) to prepare for medical
school. After his first session in medical school, he came back to visit
in Eugene, to say that something was happening to his brain, and he
wanted me to remind him, essentially, who he was, or had been. Now
(after that, he didn't return to Eugene) he's an established plastic
surgeon in NYC. In the 1970s there was a program on public television
that documented a woman's experience beginning with her diagnosis of
cancer. As she learned that it wasn't curable, and that there would be
great pain, she asked her doctor if she shouldn't leave the country to
go to England where she could get the Brompton cocktail,
cocaine-morphine-ethanol, but the doctor assured her that she didn't
need to leave, because she would be given all the drugs she needed for
pain control. The last part of the video showed her pleading with the
doctor, who was explaining that he mustn't let her get addicted, and
then it ended with her shrieking and moaning, with unrelieved pain until
she died. The emotional plague takes different forms in our society,
the medical profession is just one form.

 

[PeterSN]

[2022]
[me] Hey Dr Peat,
I was wondering if there is any relationship between the gut and the lungs/heart and how well they function in relation to gut health.

I've noticed the more starch and fermentable fibers i eat the worse my breathlessness and heart palpitations, maybe there is a relationship to endotoxin, excess serotonin, estrogen and histamine?

[Ray] The connection is very close. A clean intestine helps.

 

[PeterSN]

[2022]
[Me]
Hey Dr Peat,
I'm curious are there any downsides or concerns when utilising the carrot salad on a person with sensitive digestion ( just asking as my Raynaud's/erythromelalgia has increased after the carrots)?

[Ray] Too much carotene can be a problem if your thyroid function is low.

 

[PeterSN]

[2022]
[Me]
Dear Dr Peat,

I have been having a lot of heart arrythmias for years now, they get much worse when I'm bloated and gassy, my average HR is 61 BPM for the day, temperature around 36.1 - 37 degrees usually.

I was wondering if you could suggest any fixes?

[Ray]
Have you had blood tests? What are your main foods?

[Me]
I did get a TSH blood test which came back around .5

My main foods at the moment are 150g parmasan cheese, 2 bananas, 1 cup white rice, 2 cups milk, 4 tbsp irradiated honey, 4 tbsp white sugar, 200g beef mince and 2 fried eggs.

I am also getting really bloated with cold hands and feet in the evening, I'm also prone to panic attacks if I don't drink enough milk and sugar(which bloats me the most)

I am also getting some kind of erythromelalgia in my hands and feet, especially happening in the evening.

I haven't been getting a lot of sun lately and am extremely anxious around other people who aren't my family(like friends)

I used to be on the carnivore and keto diet a year ago, doing that for 1.5 years. I did get a blood test when I was on carnivore, feeling really stressed. My LDL cholesterol came back sky high with very low triglycerides.

Then I started doing a diet with the foods that you promote, fruit, honey, sugar, Haagen Das i ce cream, etc. Have been doing that since March 2021, and I feel my autoimmune symptoms and heart arrythmias, as well as bloating, has gotten worse.

There was one instance where I was on a plane and had eaten a whole bag of raw carrots the day prior with no evacuation afterwards even on the plane the day after, I still had the carrots in me. I then drank alot of orange juice, and the bloating and heart arrythmias were so bad i had to stand for most of the flight(8 hrs).

[Ray]
I think it would help your thyroid fuction to reduce the meat and eggs and bananas, and have more milk and easily assimilated carbohydrates, such as orange or concord grape juice and oat bran.

 

[PeterSN]

[2022]
[Me]
Would grapefruit be ok?

[Ray]
Yes, if they are ripe and sweet.

 

[Evolutionarily]

[2020]
I am trying out a low-dose of Penicillin, ~50mg couple times a day, for intestinal bacterial overgrowth, and I was wondering do you think it is a good idea to continue to supplement bacteriophages (Life Extension Florassist) during this time, or discontinue until finished? Thanks.

[Ray]
I don’t think there would be any harmful interaction.

 

[Evolutionarily]

[2022]
<Some details about low breastmilk production and declining rate of weight gain in baby>

What is best in your opinion? Goat's milk? A formula made from goat's milk powder or cow's milk powder? Does anything else need to be added (lactose, colostrum, ghee/coconut oil, etc)? Thank you very much in advance.

[Ray]
I know people who bought frozen human milk as a supplement. With any powdered milk it’s important to find out whether an anti-caking agent was used in making it. If the mother’s thyroid and vitamin D levels are good, drinking 2 to 3 quarts of milk and a quart or two of sweet orange juice per day will usually quickly increase milk production and quality.

Any dehydrated milk product is going to contain some oxidized materials, but as a small addition to breast milk it should be o.k.

 

[Evolutionarily]

[2020]
I currently have an infection and have been prescribed Ciprofloxacin Ear Drops. I wanted to email you to ask your opinion on topical application of Ciprofloxacin, since many feel this is not a good antibiotic. Would advise against it (and try something else first), or is short term topical application fine to remove infection?

[Ray]
Systemic risk is small when it’s used only in the ear, but I think it’s best to try one of the old safer antibiotics first—tetracycline, penicillin, erythromycin or azithromycin.

 

[Evolutionarily]

[2021]
I have to get a chest x-ray next week, 2-3 days after an international flight.

Is there anything I can do to help mitigate any potential damage/stress?

[Ray]
Aspirin, thyroid, and progesterone.

 

[Evolutionarily]

[2022]
Our 8 month old son is still breastfeeding, and started eating solid foods. We are feeding him what we are eating, meat (including liver), fruit, seafood (including cooked oysters), potatoes, occasional amounts of white rice and sourdough bread.

Is there anything else you think is optimal for a child this age? Cows milk? Carrot salads? Anything else?

[Ray]
I think following his interests is o.k., but not going too fast.

[Reply]
When you say not going too fast, do you mean moving slowly with the quantity of food? He is still breastfeeding multiple times during the day and throughout the night.

[Ray]
I mean not introducing new foods too frequently before a year.

 

[Energizer]

[2012]
Q:

How malleable is intelligence?

RP:

"In 1962 Mark Rosenzweig showed that an enriched environment caused rats' brains to grow. A little later, someone found that the DNA content of human brains kept increasing until the age of 90, and about 10 years ago, studies started showing experience-related growth in human brains. Thyroid and thiamine can have great effects on mental ability, and the steroids can either shrink or expand the brain substance. The old Weissmanist-Hayflick doctrine has kept people from thinking about the adaptive nature of adult tissues, but more people are starting to realize that the principles of embryology keep functioning throughout life."

(There were citations too, but somehow I lost them along with the original email, sorry).

 

[windinthepines]

[2014]

Me:
I might have this wrong, but I think I read somewhere that you said
people with big brains might tend to be more aware of their brain
processes. What sort of processes would they be aware of?--like how
memories are associated, how creativity works, how thoughts are
developed?--or other types of things altogether?

Peat:
The brain has a high rate of glucose oxidation, and I think a person is
likely to become aware of the effects of activities on their glucose
level when the brain's demands are very high. I think there is likely to
be a measurable difference in some of the "reflex" processes.

Personality and Individual Differences
Volume 17, Issue 2, August 1994, Pages 257–271
Sex differences in intelligence and brain size: A paradox resolved
Richard Lynn
Psychology Department, University of Ulster, Coleraine BT52 1SA,
Northern Ireland
Males have larger brains than females, even when corrected for body
size, and brain size is positively correlated with intelligence. This
leads to the expectation that males should have higher average levels of
intelligence than females. Yet the consensus view is that there is no
sex difference in general intelligence. An examination of the literature
shows that the consensus view is wrong. Among adults, males have
slightly higher verbal and reasoning abilities than females and a more
pronounced superiority on spatial abilities. If the three abilities are
combined to form general intelligence, the mean for males is 4 IQ points
higher than the mean for females. Among children up to the age of around
14 yr the sex differences are smaller because girls mature earlier than
boys. The evolutionary selection pressures responsible for greater
intelligence in males are discussed.

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

Personality Predicted by Size of Different Brain Regions
Rachael Rettner | June 23, 2010 06:39am ET

In a social situation, it's easy to tell the difference between a
wallflower and the life of the party, but a new study suggests we can
also spot differences in their brains.

The results show the size of certain brain regions is related to
people's personalities. For instance, highly altruistic people had a
bigger posterior cingulated cortex, a brain region thought to be
involved in the understanding of others' beliefs. Bigger regions are
assumed to be more powerful. [Top 10 Mysteries of the Mind]

"One of the things that this shows is we can start to develop theories
about how personality is produced by the brain," said study researcher
Colin DeYoung, of the University of Minnesota.

While people's personalities are likely shaped by both genetic and
environmental factors, the findings might help explain the differences
in people's actions and demeanors from moment to moment, he said, or
"what produces the patterns of behavior and emotion and thought that we
describe as personality."

The big five

There are many ways to describe someone's character — from talkative to
anxious to hardworking and organized. Psychologists have found that many
traits often go together and have grouped these traits into five
overarching categories — extraversion, neuroticism, agreeableness,
conscientiousness and openness/intellect.

Psychologists can get a pretty good picture of someone's personality by
determining to what degree they express each of these traits. [Read:
Personality Set For Life By 1st Grade]

Scientists have only recently begun to link up personality research with
neuroscience to try to figure out the underlying brain mechanisms
responsible for personality differences.

DeYoung and his colleagues imaged the brains of 116 participants who had
previously completed a questionnaire designed to assess their
personality in terms of the "big five."

Next, they matched up all the brain images. Since everyone's brain is
different, the images won't line up perfectly right off the bat. So the
researchers picked one image — from a participant who scored about
average for all five traits — to serve as a "reference brain."

A computer program was then used to squish and stretch the images so
that they all lined up with the reference brain. This allowed the
researchers to compare all the subjects' brains, and see how large or
small certain brain regions were relative to one another.

Personality in the brain

A connection between brain region size and personality was found for
four out of the five traits (all except openness/intellect).

Those who scored high on neuroticism — which indicates a tendency to
experience negative emotions, including anxiety and self-consciousness —
was associated with a larger mid-cingulate cortex, a region thought to
be involved in the detection of errors and response to emotional and
physical pain. Neurotics also had a smaller dorsomedial prefrontal
cortex, a region implicated in the regulation of emotions. [Read: Why
Neurotics Haven't Died Out]

Extroverts, those who are sociable, outgoing and assertive, had a larger
medial orbitofrontal cortex, a region involved in processing rewards.
This goes along with the idea that extroverts are sensitive to rewards,
which in our society often involve social interactions and status.

Conscientious people, who tend to be orderly, industrious and
self-disciplined, had a larger middle frontal gyrus, a region involved
in memory and planning.

The researchers note however, that a bigger brain region does not
necessarily mean the region has better functioning, although extensive
evidence supports this assumption.

The results do not indicate, that people are doomed to embody one
personality or another for their whole lives. Though it's not
necessarily easy, personalities can, and do change.

"Our experience can change the brain," DeYoung said. "And as the brain
changes, personality can change," he said.

The results were published online April 30 in the journal Psychological
Science.

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

Psychol Sci. 2010 June; 21(6): 820–828.
Published online 2010 April 30. doi: 10.1177/0956797610370159
Testing Predictions From Personality Neuroscience: Brain Structure and
the Big Five
Colin G. DeYoung,1 Jacob B. Hirsh,2 Matthew S. Shane,3 Xenophon
Papademetris,4 Nallakkandi Rajeevan,4 and Jeremy R. Gray4

Abstract

We used a new theory of the biological basis of the Big Five personality
traits to generate hypotheses about the association of each trait with
the volume of different brain regions. Controlling for age, sex, and
whole-brain volume, results from structural magnetic resonance imaging
of 116 healthy adults supported our hypotheses for four of the five
traits: Extraversion, Neuroticism, Agreeableness, and Conscientiousness.
Extraversion covaried with volume of medial orbitofrontal cortex, a
brain region involved in processing reward information. Neuroticism
covaried with volume of brain regions associated with threat,
punishment, and negative affect. Agreeableness covaried with volume in
regions that process information about the intentions and mental states
of other individuals. Conscientiousness covaried with volume in lateral
prefrontal cortex, a region involved in planning and the voluntary
control of behavior. These findings support our biologically based,
explanatory model of the Big Five and demonstrate the potential of
personality neuroscience (i.e., the systematic study of individual
differences in personality using neuroscience methods) as a discipline.

Me:
So if brains with different sized parts make different personalities
and abilities, can can you see the differences reflected in head size
and face shape?

Peat:

About 40 years ago a physical anthropologist did a very good study
showing that the relative size of major brain parts can be detected on
the outside of the skull. Dogmatic antiphrenologists (pointy headed
professors) are hard to convince. Marian Diamond's book shows the
effects of estrogen-shrunken cortex vs. progesterone-expanded cortex on
the rat face; humans' relatively big cortex probably has a bigger effect
on the appearance of the face. A few years ago I asked her about
something she said in the book and she didn't have any recollection of it.