Imagine that there was a mutation [Syndrome X] that, by itself, made you ten centimeters shorter than you otherwise would be. It works by messing up iodine metabolism.
What environment influences could modify its course? Maybe growth hormone could make a difference, but that’s not super-safe.
How stable with respect to environmental variation would syndrome X be? How much money you have, where you go to school, status – the usual stuff sociologists worry about – wouldn’t make a difference. But perhaps a diet with with lots and lots of iodine – cod for breakfast, swordfish for lunch – would. So the mutation’s consequence might be entirely different in fishermen and cowboys. There’s a sense in which its effects are unstable.
Now imagine genotype Y – it makes you ten centimeters shorter, but it’s due to many small-effect mutations. Hundreds of them. No – thousands! , counting all the small-effect alleles. Maybe they’re slightly deleterious, or maybe they’re fitness-neutral (each one makes you a little shorter but does something else helpful)
These short-people alleles don’t all operate through the same mechanisms – so there are tens of different metabolic paths involved. Make that hundreds of metabolic paths, hundreds of mechanisms.
What environmental effect would strongly influence syndrome Y? Make you tall? Well, in order to do much, that environmental factor would have to influence many different mechanisms probably most of them. That’s not easy: I’d rather have to put Humpty Dumpty back together.. I suppose we could give the kid plenty of chicken* soup – it couldn’t hurt. In practice, I can’t imagine any realistic environmental factor having much influence, short of nanites programmed by tnuctipun.
*As long as it’s nobody we know.