thank for this information about temperature.

My rectal temperature is 36.8 degre in the afternoon.

In psychiatry, do you have any advantages to take high dose of iodine ?

I feel more quiet with this high dose of iodine, less brain fog !!!

From a e-book about iodine

The bottom line, however, is that the right amount of dietary
Iodide for optimum human health and happiness is about 6-
14 mg, per adult, per day. The best final dosage of Iodide
for most men is 8-12 mg. The best final dosage of Iodide
for most women is 12 mg per day. About 90-95% of
American adults can start right at those high final doses
with no health problems.
Even 1 mg per day, however, is still too high a
dosage for about 5-10% of American adults to begin with.
It may take months, or even years, for the millions of
Americans suffering from more severe thyroid problems
and/or “diabetic neuropathy” to get used to eating that
much Iodide. This is because as dying peripheral nerves
start being revived with more optimal Iodide levels and
metabolism, for months or even years, they usually still do
not function normally.If they increase their dosage too quickly, it may
cause their malfunctioning peripheral nerves to come back
to life too quickly, and thereby temporarily cause (for a
period of months) extremely intense itching and/or pain.
Even people who are just overweight, or who
suffer from an excessively rapid resting pulse rate (over 90
beats per second) also commonly have some short-term
problems adjusting to more rapid metabolism, and thus
need to go very slowly in increasing their dosage. It turns
out that most people with high pulse rates actually have
slow metabolism, due to poor general activation, and/or
use, of Thyroid Hormones. Their hearts usually run too
fast because they have high levels of the inactive Thyroid
Hormone, T4, and the heart is better at activating and using
T4 than the rest of the body is.

The publicly un-proclaimed Iodide
supplementation program of the 1960’s was also associated
with reductions in the rates of cancer and cardiovascular
diseases, with generally improving intelligence, emotional
health, and happiness, and with increased capacity to fall
and stay in love, in both men and women. Recall that those
adults under that age of 30 during the 1960’s, and those
who came of age during the 1960’s, were called “The Love
Generation,” “Free Lovers,” “Digger,” and “Flower
Children.” With the increased level of dietary Iodide
during the 1960’s, Americans ended up with the highest
birth rates and marriage rates in American history, and the
lowest divorce rates (as a percentage of marriages) since
the 1920’s.

For the time being, let me just assert that ½ mg of
Iodide per day is still so little that most older people will
hardly notice any difference right away. In fact, that may
be why the famous “generation gap” developed during the
1960’s. Generally speaking, older people did not get as
much dietary Iodide as younger people because they ate
less baked goods. Also with the lower Melatonin levels
and higher sex hormone levels in the elderly, they were not
as sensitive to what whatever Iodide they did get. Thus,
they continued with their grumpier attitudes and in their
older more materialistic ways, while the young generation
felt happy, carefree, fell in love, had children and got
married at record rates. The older generations could not
understand why so many teenagers were throwing
prudence to the wind, falling in-love, getting pregnant and
getting married. The younger generation could not
understand what had made their parents so cold and
materialistic. They could not understand why their parents
did not know that love is the most important thing in life.
Whether or not the young got more Iodide than
their parents during the 1960’s, they had lower sex
hormone level because of their youth and higher Melatonin
levels, so they were much more sensitive to, and affected
by, even slightly higher levels of Iodine. When you have
low sex hormone levels going in, just a little more Iodide
than the average American is getting today can speed-up
your metabolism and Progesterone production. That in
turn can very significantly further suppress your sex
hormone levels, and thereby delay the onset of puberty,
improve and extend the development of intelligence by
delaying and extending puberty, intensify and extend
romantic feelings during and after puberty, and enhance
and maintain the ability to fall and stay overwhelmingly in
love.

thank

the e-book of Ford Lewis

http://lewisford.info/files/The_Basic_Program_from_Feeling_Young_and_In_Love3.pdf

more study

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)

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.

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.

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. michael.zimmermann@ilw.agrl.ethz.ch
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

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. 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.

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.

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.

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.