query about thyroid antibodies

[haggisplant]

Do thyroglobulin antibodies have any affect on conversion or utilisation of t4/ t3 or do they just affect the thyroid gland?

[greygoose]

They don't affect anything, really. Their job is to come along after an immune system attack on the thyroid (no, they don't attack the thyroid themselves), and signpost traces of TPO and Tg that have leaked into the blood, so that they can be taken away and destroyed. Because they're not supposed to be in the blood.

So, effectively, the antibodies just keep the blood clean, nothing to do with conversion, T3, T4 or the thyroid itself.

[haggisplant in reply to greygoose]

have I said the right term? Anti thyroglobulin? Why do medichecks test for it then?

[greygoose in reply to haggisplant]

Yes, you used the right term. But the answer is in the name, really: ANTI thyroglobulin. Antibodies are exclusive, they are only attracted by one thing and ignore everything thing else. So, if there is thyroglobulin in the blood, where it shouldn't be, the Tg antibodies are attracted to it.

And the fact that they are there in force, means that there is thyroglobulin in the blood, which means that the thyroid has suffered and attack allowing it to leak out of the thyroid cells, which in turn means that you have an autoimmune disease: Hashi's or Ord's. So, positive Tg or TPO antibodies = autoimmune thyroid disease. That's why we test for them.

[radd]

haggisplant

There’s plentiful research on TPOAb correlating with reduced thyroid hormone conversion but TGAb are thought to be the less aggressive regarding additional damage other than to the thyrogobulin.

However, all thyroid antibodies are unwanted inflammation and for many people lead to ‘chronic’ if they are not reduced. It is the accompanying inflammatory cytokines that directly decrease deiodinase conversion enzyme ‘D1’ activity reducing tissue T3 levels.

Inflammatory cytokines will also increase deiodinase conversion enzyme ‘D2’ suppressing TSH despite reduced peripheral T3 levels. (Yet another reason making TSH an unreliable indicator of normal tissue thyroid levels).

With all this happening deiodinase type 3 ‘D3‘ is up-regulated inflating the RT3:FT4 ratio in the blood, whilst the lowered D1 reduces RT3 clearance.

This lowering and disabling of thyroid hormones is what makes our thyroid meds work less effectively, and the chronic inflammation difficult to reduce as becomes a self-driving circle. Chronic inflammation interferes with the normal function of your cells, causes tissue damage and stimulates the immune system to release further inflammatory chemicals. There is a direct inverse correlation between CRP and reduced tissue T3 levels

[Star13 in reply to radd]

Inflammatory cytokines will also increase deiodinase conversion enzyme ‘D2’ suppressing TSH despite reduced peripheral T3 levels. (Yet another reason making TSH an unreliable indicator of normal tissue thyroid levels).

radd Thank you for that explanation . No one has ever explained that quite like that. Presumably, as I have the DIO2 defect and have always had high thyroglobulin antibodies (also occasional low high TPO) it’s the reason why my TSH has been deficient for 30 years despite forced juggling of TH, low T3 conversion and a atrophic thyroid?

[radd in reply to Star13]

Star13,

Reducing thyroid antibodies actually means trying to reduce the accompanying inflammation as they drive each other, eg quell chronic inflammatory and thyroid antibodies will (hopefully) reduce also. I have successfully used curcumin in the past and continue to follow an anti-inflammatory diet which I believe has allowed my thyroid meds to work successfully.

[Star13 in reply to radd]

Unfortunately curcumin is contra indicated for me as I’m on anticoagulants😕