Autoimmune Thyroid -Hashimoto's Disease

seek10 said:

When I take large nbr of vitamins vitamins on empty stomach, I get strange, very uneasy sensation all over the body as if some thing is blood creating this sensation. I don't know how to explain it, it is like very very very mild shock type.

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Is it any deficiency ?. Usually before sleeping I take omega -3, gaba, 5-HTP, magnesium etc. I immediatly eat some thing and it goes away almost immediatly. I was wondering whether any body faced it. This generally happens when I fast or doesn't eat any thing after 6PM to follow this nature rythm and take vitamins before sleep.

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Psyche said:

seek10 said:

When I take large nbr of vitamins vitamins on empty stomach, I get strange, very uneasy sensation all over the body as if some thing is blood creating this sensation. I don't know how to explain it, it is like very very very mild shock type.

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Does this include any supplement or is it only after specific supplements? For example, do you have it every time you take B-vitamins?

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Psyche said:

Is it any deficiency ?. Usually before sleeping I take omega -3, gaba, 5-HTP, magnesium etc. I immediatly eat some thing and it goes away almost immediatly. I was wondering whether any body faced it. This generally happens when I fast or doesn't eat any thing after 6PM to follow this nature rythm and take vitamins before sleep.

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GABA can have a reaction in some people, like "a lack of breath." Decreasing the dose might help, or taking it with a meal instead. The 5-HTP, you can take it during the day as well with meals if you feel a weird reaction on an empty stomach.

Omega 3s are best taking during the day as they can energize some people, especially if you take a bunch of them.

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Unraveling thyroid antibody tests
http://drknews.com/unraveling-thyroid-antibodies/

When it comes to thyroid antibodies, those definitive markers for Hashismoto’s, confusion sometimes arises. For instance, do your high antibody counts mean your Hashimoto’s is worse than your friend’s, whose counts are low? Or how come you first presented with negative antibodies, and now that you’re on your practitioner’s protocol and feeling significantly better your antibody counts are suddenly positive? And why is iodine producing negative antibody results? Does that mean it’s “curing” Hashimoto’s?

In this article I review thyroid antibody panels, what they really mean, how to accurately test the status of your autoimmune condition, and whether your protocol is working for you.

First of all, we all make antibodies against cell tissue. The presence of some antibodies is healthy and normal. As old tissue cells die to be replaced by new ones, the immune system tags these dead cells with antibodies, just as it would tag an invading virus or infection to destroy and remove. In the autoimmune process however, this highly organized and complex system runs awry, and antibodies tag healthy tissue. This is the case in Hashimoto’s, an autoimmune disease in which the body’s immune system tags healthy thyroid tissue for destruction and removal.

We identify Hashimoto’s by measuring thyroid peroxidase antibodies (TPO Ab) and thyroglobulin antibodies (TgAb). TPO is the most commonly elevated antibody in Hashimoto’s, however TgAb should always be checked too, even though it is not as common. To assess whether these antibodies are positive we use the lab ranges, which vary from lab to lab.

Why you can have negative antibody results and still have Hashimoto’s

Say all your symptoms point to Hashimoto’s but your antibody tests are negative. Does this mean you don’t have Hashimoto’s? Not necessarily. As you’ll learn, if your practitioner sees negative antibodies and proclaims you are “cured” of Hashimoto’s, he or she clearly does not understand some basic immune principles.

The waxing and waning immune system

When I have a patient who is struggling with symptoms of both hyperthyroidism and hypothyroidism, a strong indication of Hashimoto’s, and the antibody test comes back negative, I run a second panel. Because the autoimmune response waxes and wanes, the patient may test negative one week and positive the next. Sometimes I may even ask the patient to enjoy extra sugar and gluten in their diet before the second test, as sugar will drive up inflammation and gluten will provoke the autoimmune response, both of which better the chances of producing a positive result on an antibody lab panel.

Overall immune weakness

Some people with Hashimoto’s test negative because their overall immune health is weak and they do not produce enough antibodies. Their immune systems have been so stressed for so long that their total white blood cells and B-cells are too low to be able to make antibodies. You have to have some degree of immune fitness to produce antibodies. Many times these people will not test positive for Hashimoto’s or start to feel better until their compromised immune system improves in health.

These are the people who, after several weeks on a gluten-free diet or on a protocol from their practitioner start feeling great, yet are dismayed when a follow-up antibody panel shows antibodies are significantly higher, or are positive when they were initially negative. In some cases this is a sign that immune health has been restored to the point where antibody production kicks back into action.

TH-1 is higher than TH-2

A TH-1 dominance may be another reason for negative antibodies. As I explain in the book, we can roughly divide the immune system into two sides. TH-1 is the side that reacts immediately to an invader whereas TH-2 is the delayed response that produces antibodies. In a healthy immune system TH-1 and TH-2 are balanced, however in Hashimoto’s one of these becomes overly dominant. When TH-1 soars too high this suppresses TH-2 and hence antibody production. As a result antibody counts on a lab panel may show as low or negative. When you bring these two systems into balance, however, antibody counts on a panel may temporarily increase before balancing out.

This also explains why the use of iodine can produce a negative antibody panel in Hashimoto’s. Iodine has been shown to stimulate the autoimmune attack against the thyroid, which increases inflammation, a TH-1 response. In a TH-1 dominant person—statistically most people with Hashimoto’s—this further stimulates TH-1 while suppressing TH-2, again producing negative antibody results and giving many the impression the Hashimoto’s has been “cured.” Also, high doses of iodine can stimulate the production of TPO, the enzyme that is the target of autoimmune attack, to the point that it becomes inactive and the autoimmune attack ceases. However TPO is necessary for thyroid function and this is not a desirable approach when we have other methods that work better.

If either of these factors is a possibility, I tell people to check for inflammatory cytokine levels (the compounds that make up the TH-1 system), such as IL-2, IL-12, TNFa, and interferon. They should also check the CD4/CD8 ratio, which is the ratio between T-suppressor and T-helper immune cells. If inflammatory cytokines are high and the CD4/CD8 ratio is out of balance, this indicates an inflammatory condition that is suppressing TH-2 and perhaps artificially producing a negative result for Hashimoto’s. This is especially important to check in those using iodine to address Hashimoto’s.

(If all this immune terminology is confusing, please refer to the book, where it is explained in detail.)

Beyond thyroid antibodies to gluten

These reasons explain why Jane can have really low or even negative antibody counts and feel worse than her friend Mary, who also has Hashimoto’s but whose antibody counts are higher. Jane’s overall immune function is weaker or more out of balance. This is also why I caution people about the results from labs that test for intolerances to gluten, dairy, and other foods. A negative result does not necessarily mean you’re free to resume eating breads, pastas, and other gluten foods. In fact I heard of a woman with all the classic symptoms of Hashimoto’s, celiac disease, and rheumatoid arthritis (an autoimmune joint condition) who barely tested positive for a gluten intolerance. Unfortunately her doctor, who does not understand these immune basics, interpreted this as meaning she is only a little bit intolerant to gluten and can still eat it, just in smaller amounts, and she continues to suffer.

As I explain in the book, the Elimination/Provocation Diet is the best test for food intolerances.

Some people always test negative

Interestingly, studies also show some people always test negative for Hashimoto’s on antibody panels, while follow-up biopsies confirm that Hashimoto’s is present. That’s why it’s imperative to test other immune markers, remove gluten from the diet, and avoid iodine if Hashimoto’s is suspected.

Reacting to both TH-1 and TH-2 stimulators

In the book I explain how a challenge using designated herbal and nutritional compounds can determine a TH-1 or TH-2 dominance. One practitioner emailed with a question about a patient who reacted negatively to both TH-1 and TH-2 compounds. I have seen this before in those whose gut barrier is extremely compromised and who react to many things. In this case the focus would first be to first restore health to the gut and then try the challenge again some time later.

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Which thyroid hormone is right for you?
http://drknews.com/which-thyroid-hormone-is-right-for-you/

A question I frequently get is, “What is the best thyroid hormone?” and the answer is, “It depends!” No one magic thyroid hormone medication exists—instead a variety of factors must be considered. For instance, many people on thyroid hormones have a normal TSH but still suffer from hypothyroid symptoms. Others have a history of trying different thyroid hormones and getting different responses with each. Some do better with bio-identical (Armour), others with synthetic (Synthroid®). And for some, certain brands in either category make them considerably worse or better.

Choosing the right thyroid hormone

When choosing the appropriate thyroid hormone, three factors must be considered:

Sensitivity to fillers

Some people, especially those with autoimmune diseases such as Hashimoto’s, are sensitive to the dyes and fillers in thyroid hormone medications. Cornstarch, found in many brands, is a common trigger. Synthroid®, Westhroid, and Thyrolar contain cornstarch. A good example of how fillers can affect people occurred recently when Armour was reformulated with increased cellulose, decreased dextrose, and added cornstarch, which caused problems for many users. Nature-Thyroid appears to be the most hypoallergenic brand.

Bio-identical versus synthetic hormones

I personally prefer my patients use a bio-identical thyroid hormone such as Armour. Lab tests can measure bio-identical hormones in your system, whereas they cannot measure synthetic hormones (only TSH is an effective marker when synthetic hormones are used). However, some people clearly do better with synthetic hormones, such as Synthroid®.

Why is that? This is common in people with an autoimmune thyroid disease, especially Graves’, who have developed an autoimmune attack against T3 and T4. In other words, their immune system is attacking their thyroid hormones. Because bio-identical hormones contain both T3 and T4, this stimulates the autoimmune attack and makes the person feel worse. In these cases, a synthetic T4 may be a better option. Currently there are no lab tests to test for antibodies against T3 and T4, however one is in development.

The function of T3 hormones

T3 is the active form of thyroid hormone, having the greatest impact on metabolism, but also carries the greatest risk of overdosing. People who have difficulty converting T4 to T3, or whose cells have become resistant to thyroid hormones, do better with thyroid hormones that include T3.

However some people develop hyperthyroid symptoms with T3 support — feeling wired, nervousness, insomnia, heart palpitations, etc. This scenario is most common in Hashimoto’s patients who have constant immune attacks against their thyroid gland, which releases excess thyroid hormone into the bloodstream. These people typically do better with a T4-only medication.

Assessing responses to thyroid hormones

Many thyroid hormone users have a history of trying various meds. Some thyroid hormones make people feel wired, jittery or nervous. Others bring TSH into a normal range but do not alleviate symptoms. Some worked really well. All of these reactions provide insight into the mechanisms involved in the hypothyroidism.

No significant response, but normal TSH

This is very common with those who have Hashimoto’s. Chronic inflammation, whether it is from unmanaged Hashimoto’s or other sources (injury, surgery, infection, cancer, overtraining), can cause three scenarios:

* Prevents the conversion of T4 to T3
* Hampers communication between the pituitary gland in the brain and the thyroid gland.
* Inhibits thyroid receptors on cells from responding to thyroid hormones

In these cases, the response to T4-only medications will be poor. Another factor to consider is that the person may have many other conditions affecting thyroid health, such as insulin resistance, hormonal imbalances, gut infections, food intolerances, and more.

Only felt better with bio-identical hormones

This scenario can occur for several reasons:

* Unable to convert T4 to T3 when using T4-only medication
* Sensitivities to dyes or fillers in synthetic compounds that are not in bio-identical compounds
* May need T3 due to problems with the thyroid hormone receptors on cells
* Receptor sites on cells simply respond better to bio-identical than synthetic hormones

Only felt better with T3 combination hormones

If a person consistently does better with isolated T3 hormones, whether synthetic or bio-identical, a couple of factors are possible. One is difficulty converting T4 to T3. The other is that receptor sites on cells are resistant to thyroid hormones due to high cortisol, low progesterone, inflammation, high homocysteine, vitamin A deficiencies, and more.

Only felt better with synthetic hormones

This may occur in individuals who have an overactive metabolism and can’t tolerate additional T3. As mentioned earlier, this is common in those with Hashimoto’s who experience repeat immune attacks against the thyroid, or when the immune system is attacking T4 and T3, such as with Graves’ disease or multiple autoimmune diseases.

Felt over-stimulated with T3 or bio-identical hormones

Again, this may occur in the person with Hashimoto’s whose immune system is constantly attacking the thyroid gland, releasing excess thyroid hormone into the bloodstream. It also occurs in those with high epinephrine, an adrenal hormone, due to excess caffeine or nicotine, severe psychological stress, constant overtraining, or genetic mechanisms.

Felt fatigued and run down with thyroid hormones

This is almost always related to sensitivities to dyes or fillers in the thyroid hormone medication. It may also occur if the person is having an autoimmune response against their thyroid hormones, such as in Graves’ or in those with multiple autoimmune diseases.

Do you even need thyroid hormones?

Another factor to consider is whether you even need thyroid hormone replacement. Hashimoto’s, an autoimmune attack against the thyroid, accounts for 90 percent of hypothyroidism cases in the United States. When the autoimmune disease is successfully managed, thyroid hormones may not be needed at all, and taking them unnecessarily can do more harm than good. Another consideration is poor thyroid function caused by breakdowns in thyroid pathways that need addressing, instead of true hypothyroidism (this is discussed in Chapter Four of the book).

However if damage to the gland is substantial enough, then thyroid hormones are necessary. Not taking thyroid hormone replacement when you truly need it can have disastrous consequences on your total health and well-being. If a person shows repeated and continuous elevations of TSH, thyroid hormones should be considered.

Even when thyroid hormone replacement is used, it is still vitally important to manage the autoimmune condition. This will enhance the effectiveness of the medication, preserve the integrity of the thyroid gland, and prevent the progression of the autoimmune condition into attacks on other areas of the body.

Thyroid replacement hormones

Brand Name Thyroid Hormones

* Synthroid – synthetic T4 only
* Levothroid – synthetic T4 only
* Levoxyl – synthetic T4 only
* Unithroid – synthetic T4 only
* Cytomel – synthetic T3 only
* Thyrolar – synthetic fixed ratio of T3 and T4
* Armour – bio-identical fixed ratio of T3 and T4 combination
* Westhroid – bio-identical fixed ratio of T3 and T4 combination
* Nature-Throid – bio-identical fixed ratio of T3 and T4 combination

Generic Thyroid Hormones

* Levothyroxine – synthetic T4 only
* L-Thyroxine – synthetic T4 only
* Liothyronine – synthetic T3 only
* Liotrix – synthetic fixed ratio of T3 and T4 combination
* Dessicated Thyroid – bio-identical T3 and T4 combination

Synthetic Thyroxine (T4) Hormones

* Synthroid – Brand Name
* Levothroid – Brand Name
* Levoxyl – Brand Name
* Unithroid – Brand Name
* Levothyroxine – Generic
* L-Thyroxine – Generic

Synthetic Triiodothyronine (T3) Hormone

* Cytomel – Brand Name
* Liothyronine – Generic

Synthetic T3 and T4 Combination

* Thyrolar – Brand Name
* Liotrix – Generic

Bio-Identical T3 and T4 Combination

* Armour –Brand Name
* Westhroid – Brand Name
* Nature-Throid – Brand Name
* Dessicated Thyroid – Generic

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Iodine and Autoimmune Thyroid — References
http://drknews.com/some-studies-on-iodine-and-autoimmune-thyroid-disease/

If you’re interested in some of the research that has been done on iodine and autoimmune thyroid diseases, this post is for you.

Although adequate iodine consumption is important for thyroid hormone production and iodine deficiency is the most common cause of hypothyroidism worldwide, its supplemental use in autoimmune thyroids is contraindicated. Iodine is the major cofactor and stimulator for thyroid peroxidase (TPO). TPO is the enzyme that is under attack with Hashimoto’s thyroiditis. It appears that increased iodine intake, especially as a supplement, increases the immune attack on the thyroid.(1) The extreme of this clinical expression is called the Jod-Basedow Phenomenon.(2) This phenomenon is portrayed as individuals who are iodine-deficient in conjunction with elevated thyroid antibodies. When these individuals are given exogenous iodine supplements they develop a hyperfunction autoimmune response. Although this phenomenon does take place in clinical practice at times, iodine supplementation with autoimmune thyroids does not always lead into thyroid hyperfunction. Rather one observes increased levels of TPO autoantibody levels that multiply dramatically with iodine supplements, and in many instances increased production of thyroid overactive symptoms.

In areas of the world where iodine has been added to sodium chloride (table salt), the rates of autoimmune thyroid have risen. In China, participants enrolled in a baseline study in 1999, and during the five-year follow-up through 2004, the effect of regional differences in iodine intake on the incidence of thyroid disease was examined. Of the 3761 unselected subjects who were enrolled at baseline, 3018 (80.2 percent) participated in this follow-up study. Levels of thyroid hormones and thyroid autoantibodies in serum, and iodine in urine, were measured, and B-mode ultrasonography of the thyroid was performed at baseline and follow-up. The study concluded that more than adequate or excessive iodine intake may lead to hypothyroidism and autoimmune thyroiditis.(3)

A study was conducted to evaluate the evolution of thyroid autoimmunity in relation to the change in goiter prevalence during 3 years of iodine prophylaxis in Sri Lanka. These results indicate an evolution of thyroid autoimmune markers during the course of iodine prophylaxis, which has not been described before.(4) A study evaluated the effects of iodine intake on the prevalence of thyroid dysfunction, autoimmunity, and goiter in two regions with different iodine status after two years of iodization in Turkey. In total, 1733 adolescent subjects were enrolled into the study. They measured free thyroxine (fT4), thyrotropin (TSH), antithyroid peroxidase antibodies (Anti-TPO), antithyroglobulin antibodies (Anti-Tg), and urinary iodine (UI), and examined the thyroid gland by ultrasound. The research study concluded that iodine supplementation in Turkey has resulted in the elimination of iodine deficiency in the Eastern Black Sea Region, and this has been accompanied by an increase in the prevalence of autoimmune thyroiditis and thyroid dysfunction.(5)

A study observed the effects of iodine on the level of CD4/CD8 cells and the production of thyroglobulin autoantibody (TGAb) and thyroid peroxidase autoantibody (TPO Ab), and investigated the role of iodine in thyroid autoimmunity. The study concluded that iodine might exert influence on the level of CD4/CD8, and thus the production of thyroid antibodies might directly or indirectly take part in the process of thyroid autoimmunity. Both low iodine and 100 times normal iodine intakes might activate the immune state on some degrees. The effects of iodine on immune responses of TG and TPO antigens in thyroid autoimmunity might not be completely the same.(6) A research study concluded that thyroglobulin polymorphisms, combined with the explosive mix of iodine, TPO Ab, and H2O2 necessary for thyroid hormone synthesis, inadvertently provide the trigger for the autoimmune thyroid response.(7)

A study evaluated the prevalence of chronic autoimmune thyroiditis (CAT) and iodine-induced hypothyroidism, hyperthyroidism (overt and subclinical), and goiter in a population exposed to excessive iodine intake for 5 years (table salt iodine concentrations: 40-100 mg/kg salt). This was a population-based, cross-sectional study with 1085 participants randomly selected from a metropolitan area in São Paulo, Brazil, and conducted during the first semester of 2004. Thyroid ultrasound examination was performed in all participants and samples of urine and blood were collected from each subject. Serum levels of thyroid-stimulating hormone, free thyroxine, and anti-thyroid peroxidase (TPO) antibodies, urinary iodine concentration, thyroid volume, and thyroid echogenicity were evaluated. The study also analyzed table salt iodine concentrations. At the time the study was conducted, table salt iodine concentrations were within the new official limits (20-60 mg/kg salt). Nevertheless, in 45.6% of the participants, urinary iodine excretion was excessive (above 300 microg/l) and, in 14.1%, it was higher than 400 microg/l. The prevalence of CAT (including atrophic thyroiditis) was 16.9% (183/1085), women were more affected than men (21.5 vs 9.1% respectively, P=0.02). Hypothyroidism was detected in 8.0% (87/1085) of the population with CAT. Hyperthyroidism was diagnosed in 3.3% of the individuals (36/1085) and goiter was identified in 3.1% (34/1085). The study concluded that after five years, iodine intake by the Brazilian population may have increased the prevalence of chronic autoimmune thyroid and hypothyroidism in subjects genetically predisposed to thyroid autoimmune diseases. Appropriate screening for early detection of thyroid dysfunction may be considered during excessive nutritional iodine intake.(8)

It has been reported that hyperthyroidism is associated with an altered endothelial function and increased risk of arterial thromboembolism. A study was conducted to estimate chosen markers of endothelial dysfunction in iodine-induced thyrotoxicosis (IIT). The groups studied consisted of 41 hyperthyroid subjects, who had been treated with amiodarone (n = 6) or vitamin preparations supplemented with iodine (n = 35) and 40 persons with normal thyroid function. The following parameters were measured: thyroglobulin antibodies (TG Ab), thyroid peroxidase antibodies (TPO Ab), THS receptor antibodies (TR Ab), soluble adhesion molecules: sVCAM-1 and sICAM-1, von Willebrand factor (vWF), plasminogen activator inhibitor-1 (PAI-1), C-reactive protein (CRP), fibrinogen and urine iodine concentration. RESULTS: Patients with IIT had significantly higher levels of sVCAM-1 (p < 0.01), IL-6 (p < 0.005), fibrinogen (p < 0.005) and CRP (p < 0.05) in comparison to healthy subjects, whereas sICAM-1, PAI-1 and vWF concentrations did not differ between the groups studied. The highest sVCAM-1 levels were observed in patients with amiodarone induced thyrotoxicosis, and fibrinogen and CRP–in subjects receiving vitamin preparations. There were significant correlations between sVCAM-1 concentration and the levels of sICAM-1 (r = 0.341; p = 0.029) and PAI-1 (r = 0.347; p = 0.026), as well as with urine iodine concentration (r = 0.448; p = 0.004). IL-6 concentration correlated with vWF (r = 0.456; p = 0.003), TPO Ab (r = 0.328; p = 0.036) and PAI-1 level (r = 0.319; p = 0.042). The study concluded that iodine induced thyrotoxicosis is associated with an increase of sVCAM-1 and IL-6 levels, possibly reflecting inflammatory and destructive processes in the thyroid gland. However, increased procoagulant activity was not found in patients with IIT.(9)

A study was conducted to assess the relationship between the biological exposure to iodine and hypothyroidism. METHODS: Logistic regression model was used to analyze the risk factors of hypothyroidism, according to the epidemiologic data of 3761 adults in 3 kinds of rural communities: mild iodine deficiency area (4 natural villages in Panshan County, Liaoning Province), more than adequate iodine (7 natural villages of Zhangwu County, Liaoning Province), and excessive iodine area (2 natural villages of Huanghua City, Hebei Province). The study concluded that more than adequate iodine and excessive iodine were independent risk factors of subclinical hypothyroidism (OR = 3.172 and 6.391, P < 0.05) and overt hypothyroidism (OR = 3.696 and 9.213, P < 0.05). When interactions of iodine exposure and thyroid peroxidase antibody (TPOAb) or thyroglobulin antibody (TgAb) were included, more than adequate iodine was still a risk factor of subclinical hypothyroidism (OR = 2.788, P < 0.01), but had no such effect on overt hypothyroidism. Interaction of more than adequate iodine and positive TgAb significantly affected subclinical hypothyroidism and overt hypothyroidism (OR = 2.656 and 3.347, P < 0.05). In conclusion, more than adequate and excessive iodine exposure are independent risk factors of hypothyroidism. The risk of hypothyroidism goes up and thyroid dysfunction becomes more serious with the increasing biological exposure
to iodine.(10)

The current iodine status and the impact of silent iodine prophylaxis on the prevalence of autoimmune thyroiditis among schoolchildren in a formerly iodine-deficient community in northwestern Greece were investigated. The findings were compared to those obtained from a similar survey conducted 7 years previously in the same area. A total of 302 schoolchildren (12-18 years of age) from a mountainous area of northwestern Greece were examined for the presence of goiter, and blood and urine samples were collected for assessment of thyroid function, antithyroid antibodies and urinary iodine excretion. In those children (n = 42) with palpable goiter or positive antibodies and/or a thyrotropin (TSH) level greater than 5 mU/L, thyroid ultrasonography was performed to estimate thyroid gland size and morphology. Median urinary iodine concentration in the children was 20.21 microg/dL, indicating sufficient iodine intake. Thyroid function was normal in all but 7 children, who had subclinical hypothyroidism (2.5%). Antithyroid antibodies (antithyroid peroxidase [TPO] and/or antithyroglobulin [Tg]) were positive in 32 children, including those with subclinical hypothyroidism (10.6%). Twenty-nine of these children (9.6%) also had the characteristic echo pattern of thyroiditis on ultrasound and were diagnosed to have autoimmune thyroiditis. In comparison to data from our previous survey 7 years ago, there has been a threefold increase in the prevalence of autoimmune thyroiditis among schoolchildren. In conclusion, silent iodine prophylaxis resulted in the elimination of iodine deficiency in Greece, and this has been accompanied by an increase in the prevalence of autoimmune thyroiditis.(11)

In the mountainous areas of Azerbaijan, the schoolchildren suffer from severe Iodine Deficiency (ID) with median Urinary Iodine Excretion (UIE) 36 mcg/l and prevalence of goiter 99% (estimated by US). In a population of 293,000 schoolchildren aged 8-14 y.o., a study administered capsules containing 190 mg of iodized oil (Lipiodol-Guerbet, Cedex, France) twice yearly in 6 months apart (total 380 mg). The aim of the present study was to evaluate the efficacy, the benefits, as well as the possible side-effects in a follow-up period of 6 and 12 months after the initial administration of iodized oil. Six and 12 months after the initial administration of iodide, two representative samples of 391 and 326 children respectively were examined. The evaluation included: estimation of goiter by US, determination of UIE and serum measurements of T3, T4, TSH, Tg, autoantibodies against thyroid peroxidase (anti-TPO) and thyroglobulin (anti-Tg). The results found that there was an improvement in median UIE, which increased from 36 mcg/l to 68 and 81 mcg/l after 6 and 12 months of treatment respectively. The prevalence of goiter decreased from 99% to 54% and 26% respectively. Tg was decreased at 6 and 12 months from the first administration, whereas TSH remained unchanged at 6 months and decreased at 12 months when compared to the latter value. Hypothyroidism was detected in 7% of children after iodide administration both at 6 and 12 months, but overt hypothyroidism was observed only in 0.5% at 12 months. Subclinical hyperthyroidism was detected in 2% and 6% after iodide administration both at 6 and 12 months. There was a significant increase in the title of thyroid auto antibodies in 6 months, which was retained and increased in 12 months. There was no relation between the appearance of thyroid dysfunction and the positive thyroid auto antibodies. It was concluded that the dose of 190 mg iodide administered twice yearly, improved iodine deficiency and endemic goiter in schoolchildren. The increase of UIE resulted from iodide administration, was accompanied by an increased title of thyroid auto-antibodies and an increased prevalence of hyper and hypo-thyrotropinemia apparently of no autoimmune etiology.(12)

Lifelong thyroid hormone replacement is indicated in patients with hypothyroidism as a result of Hashimoto’s thyroiditis. However previous reports have shown that excess iodine induces hypothyroidism in Hashimoto’s thyroiditis. A study investigated the effects of iodine restriction on the thyroid function and the predictable factors for recovery in patients with hypothyroidism due to Hashimoto’s thyroiditis. The subject group consisted of 45 patients who had initially been diagnosed with hypothyroidism due to Hashimoto’s thyroiditis. The subjects were divided randomly into two groups. One group was an iodine intake restriction group (group 1) (iodine intake: less than 100 micro g/day) and the other group was an iodine intake non-restriction group (group 2). The thyroid-related hormones and the urinary excretion of iodine were measured at the baseline state and after 3 months. After 3 months, a recovery to the euthyroid state was found in 78.3 % of group 1 (18 out of 23 patients), which is higher than the 45.5% from group 2 (10 out of 22 patients). In group 1, mean serum fT4 level (0.80 +/- 0.27 ng/dL at the baseline, 0.98 +/- 0.21 ng/dL after 3 months) and the TSH level (37.95 +/- 81.76 micro IU/mL at the baseline, 25.66 +/- 70.79 micro IU/mL after 3 months) changed significantly during this period (p < 0.05). In group 2, the mean serum fT4 level decreased (0.98 +/- 0.17 ng/dL at baseline, 0.92 +/- 0.28 ng/dL after 3 months, p < 0.05). In the iodine restriction group, the urinary iodine excretion values were higher in the recovered patients than in non-recovered patients (3.51 +/- 1.62 mg/L vs. 1.21 +/- 0.39 mg/ L, p=0.006) and the initial serum TSH values were lower in the recovered patients than in the non-recovered patients (14.28 +/- 12.63 micro IU/mL vs. 123.14 +/- 156.51 micro IU/mL, p=0.005). In conclusion, 78.3% of patients with hypothyroidism due to Hashimoto’s thyroiditis regained an euthyroid state iodine restriction alone. Both a low initial serum TSH and a high initial urinary iodine concentration can be predictable factors for a recovery from hypothyroidism due to Hashimoto’s thyroiditis after restricting their iodine intake.(13)

A study looked at the effect of iodine on autoimmune thyroiditis. Autoimmune thyroiditis is an organ-specific autoimmune disorder characterized by infiltration of the thyroid gland by lymphocytic inflammatory cells, often followed by hypothyroidism due to destruction and replacement of the follicular tissue. Dr. Noel Rose and members of his laboratory at Johns Hopkins University have continued to study autoimmunity using autoimmune thyroiditis as a model. Autoimmune thyroiditis is multifactorial, with both genetic and environmental factors involved. We have studied familial association of thyroid antibodies in juveniles with either autoimmune thyroiditis or Graves’ disease. Epitope analysis of thyroglobulin autoantibodies showed that autoantibodies from unrelated patients with disease had greater similarity of epitope binding than members of their own family. Subclass analysis of thyroglobulin autoantibodies indicated that IgG2 was dominant in autoimmune thyroiditis. Much of our work focused around iodine as an environmental trigger of autoimmune thyroiditis. We showed that iodination of the human thyroglobulin molecule alters its immunoreactivity. We explored the role of excess iodine ingestion in exacerbating thyroiditis using the NOD.H2h4 mouse as a model. We found multiple effects of excess iodine, including changing the immunogenicity of the thyroglobulin molecule and the upregulation of ICAM-1 and ROS in the thyrocyte itself. These observations may help to delineate the mechanisms by which iodine exacerbates thyroiditis and to explain differences in the host response of genetically susceptible individuals compared to those who are resistant to disease.(14)

Citations

1 SurksM, Sievert R. Drugs and thyroid function. NEJM, 1995;333(25):1688.

2 Weetman A. Graves’ Disease. NEJM 2000;343(17):1236.

3 Effect of iodine intake on thyroid disease in China. N Engl J Med. 2006 Jun 29;354(26):2783-93.

4 Evolution of thyroid autoimmunity during iodine prophylaxis0the Sri Lankan experience. Eur J Endocrinol. 2003 Aug;149(2)103-10.

5 High prevalence of thyroid dysfunction and autoimmune thyroiditis in adolescents after elimintion of iodine deficiency in the Eastern Black Sea Region of Turkey. Thyroid 2006 Dec;16(12):1265-71.

6 Experimental study on effects of iodine deficiency and excess on thyroid autoimmunity. Zongua Yu Fang Xue Za Zhi. 2006 Jan;40 (1):18-20.

7 Why measure thyroglobulin autoantibodies rather than thyroid peroxidase autoantibodies? Thyroid 2004 Jul;14(7):510-20.

8 Camargo RY, Tomimoria Ek, Neves Sc, et al. Thyroid and the environment: exposure to excessive nutritional iodine increases the prevalence of thyroid disorders in Sao Paulo, Brazil. Eur J Endocrinol. 2008 Sep;159(3):293-9.

9 Zonenberg A, Tolejko B, Scelachowska M, et al. Markers of endothelial dysfunction in patients with iodine induced hyperthyroidism. Endokryonol Pol. 2006 May-Jun;57(3):210-7.

10 Chong W, Shit Xg, Teng WP, et al. Multifactor analysis of relationship between the biological exposure to iodine and hypothyroidism. Zhongua Yi Za Zhi. 2004 Jul 17:84(14):1171-4.

11 Zois C, Stavrou I, Kalogera C, et al. High prevalence of autoimmune thyroiditis in school children after elimination of iodine deficiency in northwestern Greece. Thyroid. 2003 May;13(5):485-9.

12 Markou KB, Georgopoulous NEA, Makri M, et al. Improvement of iodine deficiency after iodine supplementation in school children of Azerbaijan was accompanied by hypo and hyperthyrotropinemia and increased title of thyroid autoantibodies. J Endocrinol Invest. 2003;26(2 Suppl):43-8.

13 Yoon SJ, Choit SR, Kim DM, et al. The effect of iodine restriction on thyroid function in patients with hypothyroidism due to Hashimoto’s thyroiditis. Yonsi Med J. 2003 Apr 30;44(2):227-35.

14 Lynne Burek C. Autoimmune thyroiditis research at Johns Hopkins University. Immunol Res. 2010 Jan 20. [Epub ahead of print]

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They are superantioxidants for cellular health and protect the cells against free radicals and oxygen stress. The status of glutathione is the single most accurate indicator of the health of a cell. Antioxidant levels become depleted in inflammatory and degenerative conditions and their depletion can create a vicious circle of further stress and degeneration. [...] The importance of optimizing glutathione reserves in immune related conditions cannot be overemphasized. [...] They are also important substrates for hepatic detoxification.

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Session 30 March 2002

Q: [Laughter] (V) Yeah I do, but it's eluded me for the moment. Dang, alright if it's gone, its gone. Hmmm, 3rd money growing density...what people will say or do, it just amazes me, blows me away. (L) It gets so bad. The more layers you peel away the worse it gets. it's like you just want to run screaming "I want out of this place." (V) I'm going to be brave here and ask if it's possible to get a symbol this evening that may work on viruses? (L) Viruses? (V) I know ...okay I'm back to the same question of consciousness.

A: Viruses make inroads only when there exists gaps in consciousness. A full field of awareness closes the gaps. Heal the soul by means of increased knowledge which leads to DNA modification which closes gaps...To do it otherwise amounts to self violation of lesson profiles elected by the self.

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Iodine is Safe and Effective

http://jeffreydach.com/2011/04/06/iodine-is-safe-and-effective-by-jeffrey-dach-md.aspx

[...]

As you know, the problem with Iodoral (iodine) relates to the patient with Hashimoto's thyroiditis with elevated TPO and/or thyroglobulin antibodies. These patients may go into Hashitoxicosis after supplementing with iodine, exhibiting hyperthyroid symptoms possibly requiring hospitalization for thyroid storm.

We are finding Hashimoto's thyroiditis to be more common than originally thought, almost epidemic, and it seems to be increasing. On a routine basis, initial evaluation includes thyroid antibody levels. In addition, all patients routinely must have a serum selenium level drawn. I have found that in almost all patients with elevated antibodies, selenium supplementation will normalize and drive down antibody levels on serial lab studies.

In order to prevent the thyroid storm and other adverse effects from iodine in Hashimoto's patients, as you know, these patients must be supplemented with selenium first. This is why we first routinely draw a serum selenium, and for those cases below 135 ng/ml, we give 200-400 meg of selenomethionune for three weeks before starting the iodine supplementation at 6.25 mg (half the 12.5 mg tab) every other day.

Starting with a lower dose of iodine avoids the various adverse effects of skin itching and metallic taste and GI symptoms that can be reported at first. These are usually transient, and after a week or so, the dose can be safely increased to a full tablet daily.

Occasionally, we see a typical Hashimoto's patient with an elevated TSH around 5 or 6, and also an upper range free T3 around 350 to 400. These patients respond to selenium supplementation well, and follow-up labs usually show free T3 coming down to the 280-300 level, which in retrospect indicates the patient initially exhibited a slight thyrotoxic effect of the Hashimoto's thyroiditis, which then cooled down after the selenium. At this point it is safe to start the iodoral. If a Hashi's patient with a slightly overfunctioning thyroid and coexisting low selenium level is then started on iodine without first optimizing the selenium level, this will aggravate the thyroiditis, and possibly throw the patient into thyroid storm.

Leaving the area of Hashimoto's and going to the general patient (with normal antibody levels without Hashi's), another big issue with iodine supplementation is that the TSH may go up, which is then interpreted by the family physician as a sign of hypothyroidism. This interpretation is an error, as the elevated TSH is cosmetic and unrelated to underlying thyroid function in these cases.

[...]

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The Effect of Dietary Lectins on Thyroid TSH Receptors

_http://livingwellnessblog.wordpress.com/2013/05/30/the-effect-of-dietary-lectins-on-thyroid-tsh-receptors/

Effects of Dietary Lectins on the Thyroid

Lectins can attach themselves to Thyroid Stimulating Hormone (TSH) receptor sites and play havoc in two ways. The first is that the Lectins are able to “fit” the receptor sufficiently enough to stimulate the thyroid but the effects are different in those with hyperthyroid or Autoimmune Hyperthyroid and low thyroid or Hashimoto thyroiditis. The second effect is that the immune response to the lectin stimulation starts an autoimmune response to the thyroid stimulating hormone (TSH) receptors on the thyroid.

What Is a Lectin?

The production of lectins, alkaloids and secondary metabolites are a defense mechanism to protect themselves and their seeds from consumption while the plant is growing and before the seeds are ready for dispersal. For the purposes of this blog the listed secondary metabolites listed below will be referred to as Lectins unless specifically mentioned. Lectins occur naturally in organic and conventionally grown vegetables and fruit. Lectins occur artificially in Genetically Modified and Selectively Bred – organically or conventionally grown vegetables and fruits.

Plant Lectin Regulation of Vegetable & Fruit Consumption

Plants invest energy into the production of seeds. Plants have evolved to encourage vegetable and fruit seed dispersal but also evolved mechanisms to decrease consumption of vegetables and fruits when unripe and from non-seed dispersing predators. To this end, plants have developed physical and chemical deterrents.

Physical deterrents:

Cryptic coloration (e.g. green fruits blend in with the plant leaves)
Unpalatable textures (e.g. thick skins made of anti-nutritive substances)
Resins and saps (e.g. prevent animals from swallowing)
Repellent substances, hard outer coats, spines, thorns.

Chemical deterrents

When immature or out-of-season, the seed, grain, vegetable or fruit are protected by chemical deterrents such as lectins to keep themselves from being eaten to extinction. Chemical deterrents in plants are called secondary metabolites, i.e. trypsin inhibitor, chymotrypsin inhibitor, α-amylase inhibitor, phytohemagluttinin (lectin), phytic acid, oxalic acid, nitrate and nitrite, L-mimosine, canavanine, L-DOPA, glucosinolates, cyanogenic glucosides/cyanogens, tannins, gossypol, chlorogenic acid, saponins, phorbol esters and alkaloids.

Damage Caused By Lectins:

They bind to the thyroid TSH-receptors acting as long-acting thyroid stimulator (LATS) stimulating the activation of TSH-receptor antibodies.
Lectins acting as LATS stimulate overproduction of thyroid hormones in those suffering from Hyperthyroid or Graves disease.
Lectins acting as LATS block production of thyroid hormones in those suffering from low thyroid or Hashimoto’s thyroiditis.
Lectins are toxic to wounded cells and inhibit the natural repair system of the GI tract.
Lectins are known to “unlock” (breakthrough) the barrier variables of the GI lining and allow large undigested protein molecules into the bloodstream.
Lectins serve as a “Trojan horse” allowing intact or nearly intact foreign proteins to invade our barrier variables (natural gut defenses) and enter behind the lines causing damage well beyond the gut and into the joints, brain and skin of affected individuals provoking cytokine immune responses.
They can bind to red blood cells causing the cells to clump together resulting in a form of anemia.
They can damage collagen and connective tissues in joints.
They are directly related to Rheumatoid Arthritis.
They can bind to the stomach lining even when the pH is 3 or less.
They stimulate abnormal thickening of the pancreas interfering with exocrine cells production of enzymes and endocrine cells production of insulin.
They stimulate abnormal thickening of the lining of the gut.
They damage the villi lining the gut.
They stimulate the shift the microbial ecology promoting the overgrowth of E. coli.
The abnormal thickening of the pancreas and gut lining plus the microbial shift exacts a nutritional penalty on the absorption of nutrition.
They can provoke IgG and IgM antibodies causing Type 2 Hypersensitivity immune responses.
They provoke a direct cytokine driven immune response causing cytokine storms, invisible illness symptoms and cytokine-induced sickness behavior.

Effects of Dietary Lectins on the Thyroid

Lectins can attach themselves to a thyroid receptor site and play havoc in two ways. The first is that the Lectins are able to “fit” the receptor sufficiently enough to stimulate the thyroid but not enough fit sufficiently to produce thyroid hormones. The second effect is that the immune response to the lectin stimulation starts an autoimmune response to the thyroid.

Thyroid stimulating hormone (TSH) at various concentrations significantly increased the response of lymphocytes to both lectins found in legumes and in other vegetables and fruit. Lectins may cause the activation of ‘long-acting thyroid stimulator (LATS)’ also known as thyroid stimulating immunoglobulins, or TSI, in the blood. TSI or LATS are antibodies that bind to special receptors on the thyroid gland than normally bind to thyroid stimulating hormone (TSH). TSH is the hormone that stimulates the thyroid gland to secrete thyroid hormones. TSIs mimic the effect of TSH, thereby causing the thyroid to secrete excess thyroid hormone. LATS mimic the effect of TSH only stimulating the thyroid but not producing any thyroid hormones.

Lectins act as Long-Acting Thyroid Stimulators (LATS) and cause the activation of Thyroid Stimulating Hormone Receptor Antibodies (TSH-R Ab). These LATS appear to act similarly to TSH after attaching to the TSH receptor. The LATS are able to “fit” the receptor sufficiently well to stimulate the thyroid while blocking the production of thyroid hormones. This activates the immune system to produce TSH-R Ab to the thyroid stimulating hormone receptors. TSH-R Ab Autoantibodies act as thyroid stimulator agonist in autoimmune hyperthyroid (Graves disease) mimicking the effects of TSH and causes the overproduction of thyroid hormones with hyperthyroid symptoms. TSH-R Ab act as TSH antagonist in autoimmune hypothyroidism (Hashimoto thyroiditis) causing an inverse reaction blocking the production of thyroid hormones making it seem as if the individual is suffering from a low thyroid.

For those with low thyroid, their TSH levels will be low but the thyroid is being stimulated resulting in swelling, tenderness and irritation to the thyroid. Those who have Hashimoto’s, hyperthyroid or Grave’s disease the TSH-R antibody will stimulate the production of TPO antibodies resulting in an immune attack on the thyroid causing further destruction. This is often the case for those with elevated TPO antibodies who are doing all the right things but still have high TPO Ab.

Lectin excited T cells, which produce immunoglobulin excited thyroid function, causing hyperthyroidism. Although pituitary TSH release is suppressed, thyroid-stimulating antibodies not subject to negative feedback maintain the hyperthyroidism. These antibodies appear to act similarly to TSH and via the TSH receptor.

Lectin Exposure Symptoms

Symptoms could be obvious, such as gas, bloating, diarrhea, or constipation (or both, alternating). Less obvious food related symptoms may include headache, fatigue, ‘indigestion,’ skin problems including hives, psoriasis, acne, swollen joints, or water retention. While some symptoms will resolve quickly after eliminating an offending family, other symptoms may take 6-12 months. Be patient. If you are genetically intolerant, you will never be able to consume that group of foods safely.

Some symptoms may occur chronically and may seem unrelated to a gut/food or lectin intolerance reactions. This group of symptoms includes the so-called degenerative diseases and autoimmune diseases like those mentioned in the list at the beginning of this report including ‘Invisible Illness,’ Cytokine-Induced Sickness Behavior, atherosclerosis, hypertension, osteoporosis, senile dementia, osteoarthritis and Rheumatoid Arthritis, inflammatory joint diseases, fibromyalgia, chronic fatigue, and adult onset diabetes. Obesity has been associated with consumption of ‘edible enemy’ lectins.

Lectin Toxicity Evades Antibody-Based Blood Tests

The type of harm lectins do is harder to diagnose than in classically defined food allergies or sensitivities. In other words, confirmation of intolerance will not be found in IgA, IgG, IgE antibody, allergy or intestinal biopsy testing because the damage done is a direct cytokine driven response, and not necessarily immune-medicated or only secondarily so. Intestinal biopsy testing may be suspect because lectins cause a thickening of the intestinal lining. The medical community is looking for thinning and damage to the intestinal lining.

The diagnostic “invisibility” is why lectin consumption is rarely linked to the ailments that afflict those who consume them. While lectins are not the sole or primary cause of a wide range of disorders, them are a major factor in sustaining or reinforcing injuries or diseases once they are initiated and/or established in the body. This response will deplete your anti-inflammatory cytokines and inhibitory neurotransmitters. Many will suffer cytokine storms during flair-ups. Some will develop into an invisible illness known as Cytokine-Induce Sickness Behavior.

Once lectins make it through a compromised mucosa and/or digestive lining. It can exert systemic effects which can easily become overlooked as being caused by eating legumes, fruits or vegetables. The best tests to determine how lectins are affecting your cytokine immune status and neurotransmitter levels are the:

Neuroscience Stimulated Cytokine Analysis Comprehensive
Neuroscience NeuroEndocrine Comprehensive

http://livingwellnessblog.files.wordpress.com/2013/05/lectin-cytokine-response.png?w=538&h=344

Four Different Hashimoto Patients – Four Different Immune Responses

All had bad reactions with the Th1/TH2 challenge. Why? All suffered a lectin driven immune response. All have an overactive Th17 immune response. Three have a suppressed TH1 response. One has a suppressed TH2 response. The upper right is immunocompromised. The lower right is immune stimulated to everything. The lower left is a raw vegan over-consuming Soft and Hard Lectins. The upper left TH1 immune system collapses when exposed to bacteria driving straight into TH17.

Systemic Effect of Lectins

Lectins may influence absorption, metabolism and systemic availability of nutrition by two different but possibly simultaneous mechanisms.

Lectins can indirectly influence hormones (the endocrine system of the body) by binding to the neuroendocrine cells of the gut and as a consequence of this input, release message molecules (hormones) to the blood. Alternatively, lectins can pass through the gut wall into the blood circulation and thus may directly influence peripheral tissues and body metabolism by mimicking the effects of endocrine hormones. The organs most often affected are the pancreas, skeletal muscle, liver, kidneys and thymus.

Thymus, spleen and other organs: Overconsumption of Soft Lectins causes the thymus and spleen to begin decreasing in size wasting away. Some of these are irreversible with potentially serious consequences for the immune system, especially T cell-mediated immunity.

Effects of Dietary Lectins on Inflammatory Cytokines

Cytokines are several different types of substances that are produced by cells within the immune system. These substances relay signals between the immune system cells. By relaying messages between the cells, these cytokines help to trigger the immune system’s response to whatever threat is present.

Lectins strikingly increase levels of multiple pro-inflammatory cytokines (especially interleukin 2 receptor (IL-2), tumor necrosis factor alpha (TNF-α), IL-6, IL-8).

Cytokines, (mediators of acute inflammation) are generated to induce cell breakdown and death. Cytokines can produce an inflammatory response to food independent of the allergic reaction that most are familiar with. Food allergy or cross-reactive testing will not detect a cytokine induced inflammatory response to food. This requires specialized testing done with the NEI Stimulated Cytokine panel that measures these cytokine and chemokines.

A phenomenon involving the function of inflammatory cytokines is known as a cytokine storm. Essentially, this is a situation where the balance of communication between immune cells and the cytokines present is interrupted.

When the inflammatory cytokines are involved in some sort of storm situation, there is a loopback created between both types of cytokines and the immune cells. The pro-inflammatory cytokines go wild – like college students on Spring Break. There are several common signs that indicate that a storm is present, including fever, body aches and nausea, along with stronger symptoms that are related directly to the ailment itself. Similar to how the college student feels after a week long binge that does not wear off.

Immune Supportive Supplements

A person is said to be immunocompromised when their immune system is incapable of working at full capacity. The immune system is how the body fights off diseases and protects itself against new infections, so someone who is immunocompromised will usually get sick more often, stay sick longer, and be more vulnerable to different types of infections. They may be more inclined to use supplements to stimulate the immune system. Until they become immune suppressed. Then they rarely get “sick.” Immunosuppressed individuals never feel well and start developing symptoms associated with Cytokine Induced Sickness Behavior (CISB).

Information from secondary sources suggests that supplementing with immune stimulating supplements, i.e. thymus gland extracts, have been shown to enhance responsiveness to Lectins and have been able to produce an cytokine storm in immunocompromised patients.

Lectins: Edible Enemies

Being realistic regarding diet is that there is always a sliding scale of lesser evils that we exchange for the experience of enjoying our foods and obtaining the comfort they provide. Because some food toxins cannot be removed from foods and other may be created during processing or cooking, consumption of small quantities of food toxins is unavoidable.

How problematic or reactive lectins are for you depends upon the health of your gastrointestinal lining, the behavior of your microflora and your immune status. If you have a Ghetto Gut where the gut lining is impaired, the microbes are misbehaving, and your ability to produce digestive chemistry is less than optimal. Any food you commonly eat will provoke a reaction including organic foods. This combination of factors will change your immune status depleting the inhibitory neurotransmitters and anti-inflammatory cytokines necessary to control the Neuro-Endo-Immune Super-system. When it comes to the immune response, small insignificant changes in lectin exposure can mean the difference between being reactive or not.

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I think that Autoimmune Diseases (probably most or all diseases?) in their root have this pattern of self violation.

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Another misconception is that iodine is contraindicated in autoimmune thyroid diseases such as Grave's disease and Hashimoto's. In reality, it is those who are iodine-deficient who are at an increased risk of developing antibodies against the thyroid gland.

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Conclusion and What I Do

Iodine and selenium are two extremely important minerals for human health, and are righly emphasized as such in the Perfect Health Diet book and blog. I believe they are fundamental to thyroid health and very important to Hashimoto’s patients.

A survey of the literature suggests that Hashimoto’s is largely unaffected by iodine intake. However, the literature may be distorted by three circumstances under which iodine increases may harm, and iodine restriction help, Hashimoto’s patients:

Selenium deficiency causes an intolerance of high iodine.
Iodine intake via seaweed is accompanied by thyrotoxic metals and halides.
Sudden increases in iodine can induce a reactive hypothyroidism.

All three of these negatives can be avoided by supplementing selenium along with iodine, using potassium iodide rather than seaweed as the source of iodine, and increasing iodine intake gradually.

It’s plausible that if iodine were supplemented in this way, then Hashimoto’s patients would experience benefits with little risk of harm. Anecdotally, a number have reported benefits from supplemental iodine.

Other evidence emphasizes the need for balance between iodine and selenium. Just as iodine without selenium can cause hypothyroidism, so too can selenium without iodine. Both are needed for good health.

A few months after I was diagnosed with Hashimoto’s I started 50 mg/day iodine plus 200 mcg/day selenium. If I were starting today, I would follow Paul’s recommendation to start with selenium and a low dose of iodine, and increase the iodine dose slowly. I would not take any kelp, because of potential thyrotoxic contaminants.

Currently I’m doing the following to try to reverse my Hashimoto’s:

PHD diet and follow PHD book and blog advices to enhance immunity against infections, since infections seems to be implicated in Hashimoto’s pathology [28][29][30]. I give special attention to what Chris Masterjohn calls “traditional superfoods”: liver and other organs, bones and marrow, butter and cod liver oil, egg yolks and coconut, because these foods are high in minerals, like iodine, zinc, selenium, copper, chromium, manganese and vanadium, all of which seems to play a role in thyroid health [31];
High dose iodine (50mg of Lugol’s) plus 200 mcg selenium daily. These I supplement because of their vital importance to thyroid and immune function;
3 mg LDN (low dose naltrexone) every other day to further increase immunity. LDN resources are listed below [32][33][34][35][36];
Avoiding mercury and other endocrine disruptors. When I removed 9 amalgams (mercury), my TPO antibodies increased for 3 months and took another 6 months to return to previous values. I also avoid fish that have high and medium concentrations of mercury. Cod consumption increased my TPO antibodies;
1g of vitamin C daily. Since it seems to confer some protection against heavy metal thyroid disfunction [37], improve thyroid medication absorption [38] and there is some evidence that it could improve a defective cellular transport for iodine [39];
Donating blood 2 to 3 times per year. In men, high levels of iron seems to impact thyroid function [40].

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Selenium supplementation is a prerequisite in all patients with elevated anti-thyroid antibody levels and Hashimoto’s thyroiditis. Iodine deficiency is a health risk and Iodine supplementation is beneficial. However, Selenium supplementation is required before giving Iodine to the Hashimoto’s patient. Selenium is inexpensive and readily available as a supplement in tablet or capsule form. The usual dosage is 200-400 mcg/day of seleno-methionine. Selenium can be toxic at excessive dosage, so it is best to measure selenium blood levels, and work closely with a knowledgeable physician.

For Iodine supplementation in autoimmune thyroiditis (Hashimotos) patients we follow a protocol described here, which starts off with selenium supplementation (200-400 mcg/d) for 2-4 weeks. After which, low dose (225mcg/d) iodine supplementation may be started.

For all other without autoimmune thyroid disease and normal antibody levels, we use Iodoral from Optimox available without a prescription on the internet. Again it is best to monitor iodine levels with spot urine iodine testing, and work with a knowledgeable physician for starting dosage.

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