Hyperthyroidism – the Basics – Grey Forest Wellness

Hyperthyroidism – the Basics

Here we are at part two of common thyroid disorders – hyperthyroidism. This is also sometimes called “thyrotoxicosis”. This generally occurs when too much thyroid hormone is produced. When we’re suspicious of hyperthyroidism we’re generally seeing symptoms that are F-A-S-T.

Metabolism (weight loss)
Temperature (heat intolerance/fever)
Heart rate (sometimes palpitations/abnormal rhythm)

Mood (agitation/anxiety)
Movement (tremors/twitches)
Digestion (diarrhea)

There are a number of symptoms beyond this, of course. Some of those include exophthalmos (protrusion of the eyes), insomnia, goiter (swelling of the thyroid gland), and abnormal menstrual cycles (loss of or infrequent cycles).

Labs

When running labs to diagnose hyperthyroidism, we’ll run the typical TSH, free T4, and ideally free T3 – just like we would for hypothyroid testing. A hyperthyroid diagnosis can come from low TSH, high T4, or high T3 levels.

You’ll recall from our discussion on hypothyroidism that optimal functional levels of TSH are around 1 mIU/L, but labs won’t diagnose low TSH until around 0.4 mIU/L. Just in case, remember that TSH (thyroid stimulating hormone) is produced by the pituitary gland, after it’s stimulated by the hypothalamus. TSH tells the thyroid gland to produce thyroid hormones – the majority of which is T4 (thyroxine), with a small amount of T3 (tri-iodothyronine).

Why?

TSH can be low for a variety of reasons.

No stimulation from the hypothalamus
Negative feedback loop from elevated T4 or T3

Elevated T4 and T3 can be due to a wide variety of reasons. Some (but not all) of which are:

Goiter (enlargement of the thyroid gland)
Thyroid or pituitary tumor
Postpartum thyroiditis (after pregnancy/childbirth)
Excess iodine
Medications
Autoimmunity

Goiter

Goiter often occurs in older women. It’s when nodules of the thyroid gland produce excess amounts of T3 or T4.

Iodine

You might recall that iodine is required for producing both T4 (4 iodine) and T3 (3 iodine). Excess iodine can lead to overproduction, but it also promotes development of autoimmune hyperthyroidism (Graves’ disease – more on that in a second).

Meds

Given that thyroid hormone replacement therapy is an art, as well as a science, it’s not uncommon that medication dosages given might be too high – leading to elevated T3 and T4. There are other medications that can cause an increase in thyroid hormone production – like amiodarone, which treats heart arrhythmias, or lithium – often used to treat mood disorders.

Autoimmunity

Graves’ disease is the most likely cause of hyperthyroidism. Graves’ is an autoimmune disorder – where the immune system attacks the thyroid gland. In Graves’ disease – we see thyroid peroxidase antibodies (TPO Ab), thyroglobulin antibodies (TG Ab), and thyroid stimulating hormone receptor antibodies (TRAb). Thyroid stimulating hormone receptors are located on the thyroid gland. TPO and TG antibodies are also found in Hashimoto’s thyroiditis (autoimmune), but TRAb is specific for Graves’ Disease.

Anything Else?

There are far fewer other factors that contribute to the development of hyperthyroidism – unlike hypothyroidism which is largely affected by nutrition, liver, and gut function. It’s a much less common condition – affecting only about 1% of the population. Whereas hypothyroidism affects about 5% of the population. Unfortunately, hyperthyroidism can be quite severe – with elevations in thyroid hormones becoming dangerous, quickly, and leading to a condition known as thyroid storm.

Thyroid storm

Thyroid storm is a condition where the thyroid hormones are alarmingly high. It’s a life-threatening condition that can occur with undiagnosed hyperthyroidism, Graves’ disease, with infections, after surgery, childbirth, or a head injury, or from medication. Imagine all of those FAST conditions listed above – on steroids. It’s a medical emergency requiring quick response.

More information coming on how to manage/co-manage thyroid disorders – including hyperthyroidism. And still more on autoimmune disorders like Graves’ Disease and Hashimoto’s thyroiditis. Stay tuned…

Light reading:

https://www.ncbi.nlm.nih.gov/books/NBK482216/

https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0142615

https://pmc.ncbi.nlm.nih.gov/articles/PMC8664564/

https://www.endotext.org/chapter/graves-disease-and-the-manifestations-of-thyrotoxicosis/

https://pmc.ncbi.nlm.nih.gov/articles/PMC8279904/

https://www.ncbi.nlm.nih.gov/books/NBK285545/

https://www.ncbi.nlm.nih.gov/books/NBK448095/

https://www.ncbi.nlm.nih.gov/books/NBK559323/

https://www.ncbi.nlm.nih.gov/books/NBK568782/

https://www.ncbi.nlm.nih.gov/books/NBK555975/

https://www.ncbi.nlm.nih.gov/books/NBK448195/