(From Janie: there’s no difference in treatment–without a thyroid or still having a sick one. You still need desiccated thyroid. Go here: http://www.stopthethyroidmadness.com/things-we-have-learned And use patient groups for more feedback: http://www.stopthethyroidmadness.com/talk-to-others )

(From Janie: Eileen, use patient groups for good feedback. http://www.stopthethyroidmadness.com/talk-to-others )

It is working fine.

If you have TRab antibodies (TSH receptor antibodies) then you *DO* have Graves disease. Graves disease is also known as “TSH RECEPTOR AUTOIMMUNITY”.

Methimazole doesn’t work on a gland that is releasing stored hormone. It only works at the first level – at the iodine molecule binding level, by preventing the creation of hormone.

HypOThyroid Graves disease is when the TRab antibodies are more potent in the “blocking” stage, and less potent in the stimulatory (TSI) phase. Getting TRab/TBII tested will often tell you if the TRab are causing you to swing back and forth from hypO to hypER and back, like Oprah is.

Methimazole also has immunomodulation effects — which can reduce TRab in as little as 4 days. If she has both type of Graves TRab antibodies, then MMI will indeed be a big help. It will reduce the TSI quickly and promptly.

Her doctor, unlike most mainstream American doctors, believes we have to get rid of the TSH Receptor Antibodies — all three types: stimulating, binding and blocking; to reduce her risk of complications down the line.

She takes a small dose of an anti-thyroid drug and at the same time thyroid replacement hormone. You see the only way to rid the body of these Graves’ related antibodies is with an anti-thyroid drug — this has been proven repeatedly in medical research studies.

My daughter has elevated TSI, TRab and TBII; her TSH is low normal with below range FT4 and mid range FT3 along with high TPOabs and TGabs. Before treatment she had very high FT3.

Likewise she was diagnosed with Graves’ disease by several doctors, but I never bought it. Her symptoms screamed hypO. Many Hashi patients have been hypEr before becoming hypO and still have blocking TSH Receptor antibodies and they also have eye problems along with various other conditions.

Mainstream medicine ignores treating thede TSH receptor antibodies other than the stimulating (TSI) antibodies. When a Graves’ patient becomes hypO just give them thyroid replacement and pretend that TED and other risk factors don’t exist.

Many HypOs still have blocking TSH receptor antibodies and will never feel well. Most hypO patients don’t know that they even have TSH receptor antibodies because they are never tested nor treated. Unless you happen upon a knowledgeable provider, like we did — which are few and far apart.

Also — Scientists recently found MANY other places in our bodies have TSH Receptor sites (not just on the thyroid). We already are aware about the eye muscle (TED) and the skin (pretibial myxedema) and acropachy (bone issues in the fingers) are seen in some cases of Graves disease when TSH Receptor antibodies attach to them. But TSH Receptors are also found on the adrenal and pituitary glands. Maybe that explains why TSH Receptor antibody positive people often have adrenal/cortisol issues and even when they are severely hyPO they have pituitary TSH suppression. Some other locations where TSH receptor sites have been found are in the bones, brain, and pancreas. And we already know that people who have TSH Receptor Antibodies can end up with thyroid encephalopathy, and diabetes.