Tag: Anti-TPO

Reducing antibodies

I believe, many thyroid patients are aware that one can do things to bring thyroid antibodies down. And that high levels of antibodies is not a good thing. You can read my post on antiodies and symptoms here. Many know that gluten is not good for us, and that selenium is good and that what we eat matters. In this post I will share with you, what science has shown really works. 

It’s important to be aware, that  people who have true Hashimotos have higher antibody levels than us with Atrophic Ord’s. Doctors call everything Hashimotos, but there are in reality many different autoimmune thyroiditis. The two most common are Hashimotos and Ord’s. Hashimotos starts with a goiter (one doesn’t need to be aware of it) and Ord’s not. In Hashimotos the gland stays large, only infiltrated by B and T lymphocytes. Whereas in Ord’s, the gland shrivels up over time.

Why do I talk about this? Because  all thyroid antibodies are produced inside the gland. By the said B lymphocytes. So as the gland atrophies in Ord’s, less and less antibodies are produced.  This means, we with Ord’s will have lower antibody levels. Often people don’t know what kind of AITD they have. But if you find it difficult to reduce your antibodies, you might have Hashimotos. Remember, we can only do our best. I have hardly any antibodies anymore, I have very little thyroid tissue left.

is absolutely necessary for hormone production. Both the TPO enzyme and the deiodinase enzymes are selenium enzymes. 

But selenium is also important for the antibody levels. I am not sure where exactely is a good selenium level. There are three Norwegian doctors who argue, that we need much higher selenium levels than what is currently advised (1). Upper reference is often 1.8 or 1.9 umol/L. These doctors argue, that upper reference should be at 3 umol /L. Toxic level is at 3.5 umol/L. I have read somewhere that high levels of Selenium can inhibit the conversion of T4 to T3, but I can’t find that study again. At least, you don’t need to worry about being a little over range. 

A safe dose is 200 mcg/day. As much as 400 mcg is considered safe. Some people eat brazil nuts for selenium. But you should be aware, that the selenium content can vary from very little to very much. I have a study on it under odds-and-ends

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Antibodies, part 1, Anti-TPO

This is part 1 in a series on anti bodies and auto immune thyreoditis. In this first part I will take a look at anti bodies in general and Anti-TPO in particular. I think you will be a little surprised at some of the findings. It’s maybe a little nerdy for some. But the main points are listed in the summary. 

This is a complex topic, and there is a lot of research going on. I will probably revise these posts as I learn more. 


All anti bodies look the same, Y shaped. They differ only on the tips of the Y. That is where they bind onto specific anti genes. People without thyroid disease can also have low levels of anti bodies, particularly Anti-TPO and Anti-TG. But whether they GET a thyroid disease later, we don’t know. A study showed, that many women had anti bodies up to 7 years before they got symptoms (1).

All antibodies are produced within the thyroid itself by B lymphocytes. So if on has little or no thyroid, one does not have high levels of anti bodies.

TPO is an enzyme that takes part in the process where Iodide gets converted into Iodine. Iodine is the form the thyroid uses in it’s hormone production. TPO can get damaged by oxidative stress. Anti-TPO then gets produced against the damaged enzyme. Oxidative stress can  start as a result of Iodine deficiency. The process has started. 

Anti-TPO is not what causes the greatest damage to the thyroid. It’s B and T lymphocytes that do that. Plus a form of the TRAb anti body, the cleavage TRAb. That can cause cell death as well. I will write about that in part 3.

One can have high levels of Anti-TPO without the thyroid decreasing in size. We call everything Hashimotos, but that is not correct. Hashimotos is the AIDT that starts with a goiter. The thyroid gets infiltrated by B and T lymphocytes, and cannot function as it should. But it doesn’t atrophy. Whereas Ord’s does not start with a goiter, and the thyroid atrophies. I will write more about that in a later part in the series.

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