Hashimoto's and antibodies

[Canis2017]

Is it possible to have Hashimoto's, but still have low antibodies of both anti-TPO and TgAb? Maybe a stupid question, but could Hashimoto's make the thyroid gland smaller?

[radd]

Canis,

Yes, it is possible as thyroid antibodies fluctuate.

Elevated antibodies not only attack our thyroid gland but cause inflammation within the body that can have a profound effect on thyroid metabolism and physiology, by suppressing the HPT axis (hypothalamus-pituitary-thyroid) and decreasing the number and sensitivity of thyroid hormone receptors & conversion of T4 to T3 (active hormone).

However, it is also possible for some people to live well with low thyroid antibodies.

[Canis2017 in reply to radd]

Thanks for you answer radd!

Very interesting - you know where I can learn more about the impact on the HPT axis? Did not understand the last sentence (my brain is working slow) - I thought low thyroid antibodies was the "normal" condition?

[radd in reply to Canis2017]

Canis,

You say you have BIG adrenal issues … Cortisol (glucocorticoids) is stimulated by ACTH from the pituitary (a little like the relationship between TSH also secreted by the pituitary and T4). Cortisol regulates blood sugar, helps regulate body fat & adapts us to stress (such as bloods sugar swings, gut dysfunction, chronic infections & auto immune disease).

A messed up HPA axis (hypothalamus-pituitary-adrenals) & faulty negative loop back can exacerbate hyperthyroidism by inhibiting enzyme (5’ deodinase) that is responsible for converting T4 to T3. It can also inhibit TSH and prevent T3 from entering the cells due to an adrenal hormone insufficiency (or iron deficiencies).

A messed up HPA axis can mess up the HPT axis (hypothalamus-pituitary-thyroid) as they work in parallel (just as cortisol and TSH should correlate). The hypothalamus gland (in the brain) monitors the levels of thyroid hormone in the body and produces TRH (thyrotropin releasing hormone) which acts on the pituitary to produce thyrotropin, aka TSH (thyroid stimulating hormone).

TSH acts on the thyroid gland to produce T4 (thyroxine) & small amounts of T3 (triiodothyronine). T4 is converted into the more active T3 by the deiodinase system (D1, D2, D3) in multiple tissues and organs. Transport proteins TBG (thyroid binding globulin) (& transthretin & albumin) carry T4 and T3 to the tissues where they are cleaved from their protein-carriers to become free T4 and free T3 to bind to thyroid hormone receptors & work their magic.

What I am saying is any adrenal issues will disrupt a whole host of things as all hormones are dependant on one another & any deficiency or elevation on one will have reprocussions further up or down the line.

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HPA axis

chriskresser.com/myth-of-ad...

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HPT axis

wellnessalternatives-stl.co...

[Canis2017 in reply to radd]

I'm diagnosed with Secondary adrenal insufficiency after testing both cortisol and adrenocorticotropic hormone (ACTH).

[Angel_of_the_North]

Hashis destroys the thyroid gland, so yes, it would get smaller, but some people are born with an under-sized gland. Antibodies can fluctuate so one normal test doesn't mean that you don't have Hashis.

[Canis2017 in reply to Angel_of_the_North]

Thanks for answering! I've tested negative for both antibodies several times, but ultrasound showed smaller thyroid than normal my age. Don't know if that could be a sign of Hashis?

I also have other autoimmune disorders, like vitiligo, and I'm a bad T4 to T3 converter. Feel I've have a tendency to alter from Hypo to Hyper symptoms, but that might be other causes like adrenal insufficiency or overdosing T3.