Hashimoto’s is an auto-immune condition. Where your body sees thyroid as “foreign” or “not self.” This stimulates production of antibodies against to your own thyroid. There are a host of auto immune conditions including Sjogren’s (Sicca Syndrome). Lupus, Scleroderma, CREST Syndrome and Rheumatoid Arthritis.
[Important note: It is vital to recognize that the TSH test is being used as a screening test. See previous blog. It will not diagnose Hashimoto’s. It will totally miss this condition for years.]
We measure two antibodies. Anti-thyroglobulin (matrix of the thyroid gland) and TPO (thyroid peroxidase). TPO is essential to the conversion of T4 to T3. Either of these can rise with Hashimoto’s. It is more common to see a rise in the TPO. This condition usually results in Hypothyroidism (under active thyroid) by interfering with the normal conversions. The normal flow is T4 converts to the active form T3. The more technical term is Hashimoto’s Autoimmune Thyroiditis. It can occasionally result in the opposite. That is, hyperthyroidism (over active thyroid) during a more acute or sub acute inflammatory phase. Thyroiditis means inflammation of the thyroid.
What causes Hashimoto’s? This is not really well known. There are various theories. You will read that there are genetic factors. And, it is far more common in women than men. It is quite unusual in men.
Let’s talk about further thyroid testing. In an effort to reduce laboratory costs and find ever cheaper methods of evaluating thyroid function, the TSH has become the more commonly accepted first line test with “reflex” follow-up.
Now this assumes three very important concepts.
The feedback mechanism between the pituitary and the thyroid is intact and functional.
It assumes a “normal distribution.” That is, a typical “bell shaped” curve of all values from low to high.
That we can assign “reasonable” upper and lower cut-off values.
Idealized Thyroid Feedback
Refer to figure 1. You can see that TSH is part of a functional feedback loop. High values infer hypothyroidism (under-active thyroid) and low values infer hyperthyroidism (over active thyroid). The TSH values are opposite (inverse) to thyroid activity. A compensatory mechanism.
But there is human variation. It is an idealized loop that is not as precise as an integrated circuit. A result of overly simplified mechanistic thinking. There are rare situations where hypothalamic dysfunction can cause very low TSH levels rather than feedback from low thyroid activity. This is termed central hypothyroidism.
We have steadfastly maintained over the last 15 years that complete thyroid analysis should include a TSH, free T4 and a free T3. Frequently adding the reverse T3 and thyroid antibodies. Refer to our previous post. The TSH is a poor measure of free T3 — the active metabolite or driver of metabolic function.