A Primer on Thyroid Dysfunction

This blog post accompanies the 6th episode of my BioBros Podcast, featuring Derek of More Plates More Dates and Vigorous Steve. During the episode, I discuss thyroid function because (1) both Dallas the alleged growth hormone abusers Dallas McCarver and Dave Palumbo developed it, and (2) GH use lowers TSH levels in most people. Until now, it is my impression that no one in the PED or biohacking community has ever explained how growth hormone lowers TSH, and whether it is dangerous for the thyroid.

Without knowing anything about thyroid function, I assumed that pro-growth forces could accelerate cancer development, leading me to conclude upregulating TSH chronically could produce hyperplasia. It turns out that I was right, but the situation is much worse than that. And who knew that cabergoline/pramipexole are potent growth hormone inhibitors?


1. Hypothalamus releases thyrotropin-releasing hormone (TRH).

a. Binds to the thyrotropin-releasing hormone receptor (TRHR) in the anterior pituitary.

2. Pituitary releases thyroid-stimulating hormone (TSH) into the bloodstream.

3. TSH stimulates the thyroid to produce thyroxine (T4) and triiodothyronine (T3), which stimulates the metabolism.

4. T3 and T4 act via somatostatin to inhibit hypothalamic TRH in a negative feedback loop.


1. Chronic TSH stimulation can produce hyperplasia of the thyroid gland[1][2].

2. Catecholamines: not fully understood, except at the dopamine receptor.

a. Norepinephrine[3] stimulates the release of TRH from the hypothalamus, which is likely how the cold speeds up our metabolism faster.

b. Dopamine regulates TSH[4].

i. Dopamine[5] and dopamine receptor agonists[6] suppress TSH synthesis while dopamine antagonists[7] minorly enhance TSH synthesis.

1. Schizophrenics have higher T3[8] and T4[9] levels.

ii. Note that dopamine may lower GH[10] pulses.

1. Dopamine agonists are used to treat gigantism, inhibiting GH more effectively than IGF-1[11] - think of using nandrolone sans GH now!

2. Acutely, they cause growth hormone release in healthy people[12].

3. IGF-1:

a. Type 1 IGF-1 receptor is mostly expressed in the thyroid gland[13].

b. IGF-1R overexpression in the thyroid increases gland weight, decreases TSH, increases serum T4, suggesting that IGF-1 and the IGF-1R stimulate thyroid function[14].

c. Epidemiologic studies reveal IGF-1 levels are associated with goiter[15].

d. In acromegaly:

i. Acromegalic people have increased thyroid vascularity[16].

ii. In a study of 62 Italian acromegalics: thyroid volume is associated with the duration of acromegaly, 78% of patients had thyroid disorders (particularly non-toxic nodular disorder), and thyroid carcinoma was more common[17].

iii. A study of 37 acromegalics found goiters to be common.

1. Early in the course of the disease, a diffuse goiter develops.

2. Thyroid autonomy and nodule formation begin – growth can continue without TSH.

3. Attenuating GH secretion can reduce thyroid size, but this is limited by the extent of nodularity[18].

e. In hypopituitary patients given GH, IGF-1 does not independently stimulate thyroid growth but enhanced proliferation of thyroid cells by potentiation the mitogenic effects of TSH.

f. In women[19] but not obese[20] people, GH administration suppresses TSH.

g. IGF-1 levels are dose-dependently associated with the risk of thyroid enlargement and nodule formation in non-acromegalic people[21].


1. When iodine sufficient, about 5% of people have thyroid nodules, though 68% harbor occult nodules.

2. 65% with ultrasound, 15% with CT or fMRI, and 1-2% with positron emission tomography (PET).

3. Solitary in 50% of cases.

4. More nodules in older people, females, and larger people.

5. 16 million Americans have a palpable nodule: about 10% have cancer, 5% cause compressive problems, and 5% cause thyroid dysfunction.


1. 211% increase from 1975-2013, 3% annually.

2. Most new diagnoses are of papillary thyroid cancer (PTC), the least aggressive and most common type.

3. Doctors hypothesized that over-surveillance of small tumors that would not cause pathologies may be responsible.

4. This meta-analysis finds a