I found this in a book where it talks about iodine and hashis

[Guest guest]

Someone just posted this site and this part comes from a book on the site

that explains Hashi's. What does everyone take from it?

_http://www.thyroidmanager.org/Chapter8/8-frame.htm_

(http://www.thyroidmanager.org/Chapter8/8-frame.htm)

Iodide Metabolism and Effects

Many patients with Hashimoto's thyroiditis do not respond to injected TSH

with the expected increase in RAIU or release of hormone from the gland(81).

These findings probably mean that the gland is partially destroyed by the

autoimmune attack and is unable to augment iodine metabolism further. Further,

the

thyroid gland of the patient with Hashimoto's disease does not organify

normally(82) (Fig. 8-4). Administration of 400 mg potassium perchlorate 1 hour

after giving a tracer iodide releases 20 - 60% of the glandular radioactivity.

Also, a fraction of the iodinated compounds in the serum of patients with

Hashimoto's thyroiditis is not soluble in butanol, as are the thyroid hormones,

but is an abnormal peptide-linked iodinated component. This low-weight

iodoprotein is probably serum albumin that has been iodinated in the thyroid

gland.

A similar iodoprotein is also found in several other kinds of thyroid

disease, including carcinoma, Graves' disease, and one form of goitrous

cretinism.

It may be formed as part of the hyperplastic response. TG is also detectable

in their serum.

Iodide is actively transported from blood to thyrocytes and recently the

sodium / iodide symporter (NIS) has been cloned. Antibodies against NIS were

found in autoimmune thyroid disease(83). This antibody has an inhibitory

activity on iodide transport and may modulate the thyroid function in

Hashimoto's

thyroiditis. More recent studies reported rather low prevalence (less than 10%)

of anti-NIS antibodies in Hashimoto's disease and clinical relevance is

still unknown(84),(85).

In animal experiment iodine depletion prevents the development of autoimmune

thyroiditis(86). It is suggested that mild iodine deficiency partly protect

against autoimmune thyroid disease(87), although it is controversial(88). In a

region where iodine-containing food (such as seaweed) is common, as in

Japan, excessive dietary iodine intake (1000 micro g/day or more) may cause

transient hypothyoidism in patients with subclinical autoimmune thyroiditis.

This

condition is easily reversible with a reduction in iodine intake(89). Iodine

is important not only for thyroid hormone synthesis but also for induction and

modulation of thyroid autoimmunity. In general, iodine deficiency

attenuates, which iodine excess accelerates autoimmune thyroiditis in

autoimmune prone

individuals(90). In animal experiment, it is revealed that enhanced

iodination of thyroglobulin facilitates the selective processing and

presentation of a

cryptic phatogenic peptide in vivo or in vitro. Moreover, it is suggested

that iodine excess stimulates thymus development and effects function of

various immune cells(91).

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