Too much GH: gigantism vs. acromegaly
Excess GH almost always comes from a benign pituitary tumor. What it does to the body depends entirely on one thing from Guide 2: are the growth plates open or closed? If GH excess begins in childhood, while growth plates are still open, the long bones keep lengthening and the person becomes extremely tall — this is gigantism.
If the same GH excess begins in adulthood, after the plates have fused, the bones can no longer grow longer — so they grow thicker and broader instead. Hands and feet enlarge, the jaw and brow coarsen, rings and shoes stop fitting. This is acromegaly. Same hormone, same tumor; the only difference is whether the plates were still open. Treatment targets the tumor, often with surgery and sometimes a somatostatin analog to mimic the natural brake.
Too little: GH deficiency and short stature
On the other side, growth hormone deficiency in a child shows up as slow growth velocity and falling percentiles — the slope flattening that Guide 2 warned about. Because GH is pulsatile, diagnosis relies on a low IGF-1 plus stimulation testing rather than a single GH level. When real, it is treatable with daily GH injections, and the earlier it is started, the better the final height.
Too early, too late
Precocious puberty means the changes arrive much earlier than expected — for example, breast development or testicular enlargement in a very young child. The danger is not only social: early sex hormones accelerate bone age and fuse the plates ahead of schedule, so a child who is tall now can end up a short adult. When it is central (driven by an early-waking GnRH axis), the elegant fix is a GnRH analog given continuously — which, recalling Guide 3, switches the pituitary off by removing the pulse, pausing puberty until the right age.
Delayed puberty is the opposite: no signs by an age when most peers have started. By far the most common cause is constitutional growth delay — the healthy late bloomer. These children are short and immature for their age but have a delayed bone age that matches their delayed development; their internal clock is simply set later, often running in families, and they catch up to a normal adult height on their own. The hard part is patience: distinguishing this benign pattern from a true deficiency is one of the central skills in pediatric endocrinology.
GH excess + plates OPEN → GIGANTISM (very tall) GH excess + plates CLOSED → ACROMEGALY (broad, not tall) GH deficient (child) → slow velocity, short stature (treatable) Puberty too EARLY → precocious puberty → bone age races, plates fuse early Puberty too LATE, healthy → constitutional delay → bone age delayed, catches up