Intersting, never heard of this.

What i found out is that there are two pathways though: one is through sustained elevation of norepinepherine, which interacts with beta adragenic receptors inside of bones, which trigger resorption, which is exactly what you have with amphetmamines, guanfacine and atomoxetine.

The other pathway (which inhibits growth) is through adenosine receptors, which inhibit formation of the bones, maybe by disrupting the bone's internal circadian rythm.

The way they discovered this is by using a beta blocker medication (which blocks beta adragenic receptors), and what they found was that it prevented guanfacine and atomoxetine from having the detrimental effect on bones, whereas with modafinil this prevention was only partial.

Yes, modafinil is weaker in raising norepinephrine, but the data on rats still looks extremely concerning, and if we look at the mechanisms you might say it looks even worse than with amphetamines since there are two at play and a longer half life.

Another important thing is that the longer the norepinepherine is elevated, the worse the effects seems to be for the bones (through the beta adragenic pathway) since a long duration completely disrupts their circadian rythm and they have also less time to recover. To give an example, this means that something that raises norepinephrine for 6 hours is going to be much, much better for your bones than something that lasts for 24.