The hypothalamus is the primitive site of the brain that sends either stimulating or

inhibiting hormones to the pituitary. Growth hormone stimulating hormone (GHRH)

tells the pituitary gland to secrete more growth hormone (GH). On the other side,

Growth Hormone Inhibiting Hormone (GHIH = Somatostatin) tells the pituitary

gland to stop producing more GH.

Once the pituitary receives the positive stimulating signal it then secretes GH

which in turn stimulates the liver to produce IGF-1 (Insulin-like growth factor 1) .

This is the substance that is most commonly measured as a surrogate marker for

GH output. Low IGF-1 = low GH. Somatomedin-C is just another name for IGF-1.

Depending on the lab, it might be useful to identify both to clear up any confusion.

IGF-1 is also a more stable compound unlike true GH which has up to 5 spurts a day

- the largest being just before sleep. If we were to measure GH directly it might

show as too low or too high just because of the timing. Measuring IGF-1

circumvents this problem because of its more constant blood levels. Interestingly,

both have distinct biochemical properties.

Once the IGF-1 levels are high enough, a feedback message is sent back to the

pituitary and the hypothalamus to modulate further GH secretion. This is

accomplished by secreting more Somatostatin which then slows down GH

production.

You can see the intricate play between GHRH and Somatostatin as a "servo"

mechanism in the brain to regulate just the right amount of GH release. This is the

model for virtually all brain mediated hormonal control - the thyroid, adrenals,

ovaries and testes.

Critical concept: As we age, GH output begins to fall off, whether by sluggishness

of pituitary secretion or because of true GH decline. The outcome is the same:

declining levels of GH which given rise to a plethora of symptoms which we know

are the telltale signs of aging: