Date:   1/22/2012 6:34:54 AM ( 12 y ago)
Hits:   3,020
URL:   https://www.curezone.org/forums/fm.asp?i=1902612

I don't know if this was posted already, but it is interesting to read so many correlations with thyroid autoimmunity incidence with other cumulative autoimmunity.

http://www.faim.org/chronicdiseases/autoimmunethyroid.html

Decreased thyroid activity can have many causes including anterior pituitary hypofunction, nutrient deficiency, thyroid resistance where the receptors don't respond, under conversion of T4 to T3, over conversion of T3 leading to thyroid resistance, increased thyroid-binding proteins from chronic stress, and finally from auto-immune issues such as Hashimoto's. With auto-immune disorders affecting the thyroid, it can express itself as Grave's disease when the thyroid becomes hyperactive. In this case there is not an attack on the thyroid tissue but rather an actuation of the TSH receptors, increasing the production of T4 and ultimately T3. The other auto-immune disorder is called Hashimoto's which can express itself as hyperactive or hypoactive thyroid. In this case the thyroid tissue is attacked by the immune system, begins as Hashimoto's thyroiditis (hyperthyroid) and then in later stages of the disease the thyroid becomes hypoactive. In Dr. Noseworthy's practice he sees 300 Hashimoto's cases to every one case of Grave's disease.

Interesting point above between Hashimoto's : Graves's - 300 : 1, respectively.

So what is the process involved in Hashimoto's? First the individual must have a predisposition genetically to be susceptible. Then, after an environmental trigger, there is phenotypic expression. There is a loss of thyroid tissue, lowering the thyroid hormone production and stimulating Thyroid Stimulating Hormone (TSH). Typically hypothyroidism is diagnosed. A discerning practitioner would then run an additional test to look for thyroid peroxidase antibodies (TPO ab), thyroglobulin antibodies (TGB ab) and thyroid stimulating hormone antibodies (TSH ab). If the TSH ab is the only one elevated then a diagnosis of Grave's is typical. If the TPO ab and/or TGB ab are elevated a diagnosis of Hashimoto's is typical.

In order to understand Hashimoto's it is necessary to understand the immune system and what is happening with an auto-immune response. The immune system has many feedback loops to help keep it in control. When there is an invader or perceived invader the T Helper cells are summoned. These cells call out to the NK killer cells and cytotoxic T cells which are a part of the TH-1 side of the immune system. These are kept in check by regulatory T cells which stimulate T suppressor cells once the immune response is no longer needed. The other side of the immune system is called the TH-2 side. B cells which produce antibodies are included here. In the case of auto-immune disease either the TH-1 or the TH-2 side of the immune system gets flared up. In Hashimoto's it is more common for the TH-1 side to be dominant, but sometimes the TH-2 side becomes dominant. These two sides operate much like a see-saw. If one is overactive, the other is often suppressed.

In order to effectively treat an auto-immune disease such as Hashimoto's it is necessary to treat the auto-immune dysfunction. There are known substances which support both the TH-1 and TH-2 sides of the immune system. For example, if the TH-1 side is flared up, research shows that pine bark extract, grape seed extract, green tea extract, resveratrol and pycnogenol help achieve balance. If the TH-2 side is flared up research shows that astragalus, Echinacea, glycyrrhiza, Melissa officinalis and maitake mushrooms help restore balance. It is possible, through blood testing, to determine which side of the immune system is over reacting through cytokine testing. In this way, proper nutritional support can be determined.

Anybody have experience with Hashimoto's and the above supplements to help either TH-1 or TH-2 respose?

Another key to successful treatment of Hashimoto's is to determine what triggers have caused the phenotypic expression of the genetic susceptibility. Triggers include (1)gluten intolerance, (2)too much iodine ingestion, (3)pregnancy, (4)perimenopause, (5)heavy metal toxicity, (6)gastrointestinal disorders, (7)polycystic ovarian syndrome, (8)insulin resistance and (9)deficiency of vitamin D to mention a few. The most common trigger mentioned here is gluten intolerance which is an intolerance of the gluten in wheat and flour products. There are genetic markers for gluten intolerance which will get turned on if wheat is consumed. Statistics indicate that 83% of the population in the United States carries at least one of the possible genetic markers. In almost all cases of Hashimoto's the individual carries this genetic marker and so it is always suggested that people who have been diagnosed with Hashimoto's remove all gluten products from their diet. In addition, many studies from around the world found that too much iodine and too little iodine can turn on the genetic susceptibility for Hashimoto's. As a result, typical thyroid support for a Hashimoto's patients usually is free of iodine. In the cases of pregnancy and perimenopause, it is the estrogen surges which exacerbate Hashimoto's and often give the same symptoms of menopause including hot flashes, insomnia and irritability. The patient's symptoms are treated as a hormone imbalance when actually they are the result of Hashimoto's. Gastrointestinal issues can trigger the Hashimoto's immune response as well.

1)gluten intolerance - usually means there's already an autoimmune response to gluten. I mentioned that autoimmunity of one type usually coincides with other types of autoimmunity, even if not immediate in effect.

(2)too much iodine ingestion - most of us know that this is a temporary effect for the majority of people

(3)pregnancy - not sure, but it may be temporary too

(4)perimenopause - hormones are already on the decline in this case

(5)heavy metal toxicity - most of us probably know that heavy metals can block many functions at the cellular level

(6)gastrointestinal disorders - malabsorption issues

(7)polycystic ovarian syndrome - coincides with hypothyroidism and insulin resistance

(8)insulin resistance - coincides with PCOS and hypothyroidism

(9)deficiency of vitamin D - rather, it may be vitamin D utilization, not deficiency alone.

What do you guys/gals this of the above? Additions, comments, and modifications welcome.

Also, what is your opinion of this statement: typical thyroid support for a Hashimoto's patients usually is free of iodine

Women who suffer with polycystic ovarian syndrome (PCOS) have Hashimoto's 42% of the time. PCOS sufferers battle with insulin resistance and insulin surges which trigger Hashimoto's. Insulin surges cause an inflammatory cascade of cytokines which flare the immune response. With the rise in insulin resistance (IR) in the United States population this can have a very real impact on the number of people susceptible to Hashimoto's. Insulin resistance (high blood sugar) symptoms include fatigue after meals, craving sugar after meals and difficulty falling asleep. Nutritional support for this includes sugar stabilizers and adrenal support. Of course diet and exercise play a key role, as well. Insulin surges are also prevalent in people who suffer from the hypoglycemia(low blood sugar). Hypoglycemic symptoms include energy after meals, craving sugar before meals, inability to stay asleep and a crash and craving for sweets between 3 and 5 pm. Nutritional support also addresses sugar stabilizers and adrenal support as well as diet and exercise.

42% of women with PCOS have Hashimoto's, a bold statement, but it's in the diagnostic spectrum of word play. Doctors give a diagnosis and treat the daignosis. The correlations are there however. A doctor will often check a TSH level ONLY post-PCOS diagnosis to determine thyroid status. Little do they know about the importance of other tests, including listening to the patient and seeing the symptoms of hypothyroidism first hand. It's like an off switch, they dismiss hypothyroidism post-TSH test if it's in the normal range often.

Vitamin D improves the regulatory T cell balance. It is important to check vitamin D through the 25(OH)D blood test. Sufficient levels range between 33-80 mg/ml but in the case of Hashimoto's it is recommended that a high level be maintained as many Hashimoto's patients have vitamin D receptor deficiency.

Vitamin D could become immune suppressive, lowering the autoimmune response at least in some situations initially. The D secosteroid has many functions.

Generally for treatment, Dr. Noseworthy recommends addressing all fronts necessary. Foremost to supplement with vitamin D, gut support and support for either the TH-1 or TH-2 side of the immune system, whichever one is deficient. Then he recommends detox if toxicity is a trigger, estrogen clearance if estrogen is a trigger and sugar balance if IR or hypoglycemia is playing a role.

Once Hashimoto's is diagnosed, it is irrelevant to check the TSH or the antibodies after that point. The main avenues for testing should include the T cell and B cell panel, and the cytokine panels looking at cytokines including the TH-1 cytokines (IL-2 and TNF alpha) and the TH-2 cytokines (IL-10 and IL-4) to closely watch how the immune system is responding.

From browsing through the forums and reading, I've been reluctant to post my thoughts about autoimmunity. It seems that the immune system is smart enough differentiate between healthy cells and invaders. Once you throw in a complex series of stimulating events like heavy metals, toxins, morphing bugs, and other events that can trigger an immune response, the whole game changes. The immune system starts tagging the wrong enemy. Autoimmunity cascades. Thoughts?

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