Since Ritalin is a stimulant that has been associated with caffeine at times it is worth looking into.
"We use optical techniques to measure cerebral blood volume, hemoglobin oxygenation (S(t)O(2)), and intracellular calcium ([Ca(2+)](i)) to test the hypothesis that cocaine increases [Ca(2+)](i) in the brain. The effects of cocaine were compared with those of methylphenidate[ritalin], which has similar catecholaminergic effects as cocaine (except for serotonin increases) but no local anesthetic properties, and of lidocaine, which has similar local anesthetic effects as cocaine but is devoid of catecholaminergic actions. To control for the hemodynamic effects of cocaine, we assessed the effects of cocaine in animals in which normal blood pressure was maintained by infusion of phenylephrine, and we also measured the effects of transient hypotension (mimicking that induced by cocaine). We show that cocaine induced significant increases ( approximately 10-15%) in [Ca(2+)](i) that were independent of its hemodynamic effects and of the anesthetic used (isofluorance or alpha-chloralose). Lidocaine but not methylphenidate also induced significant [Ca(2+)](i) increases[this is likely true of other tissues and not just the brain as the blood-brain barrier is the least permeable barrier in the body]] ( approximately 10-13%). This indicates that cocaine at a dose within the range used by drug users significantly increases the [Ca(2+)](i) in the brain and its local anesthetic, but neither its catecholaminergic nor its hemodynamic actions, underlies this effect. Cocaine-induced [Ca(2+)](i) increases are likely to accentuate the neurotoxic effects from cocaine-induced vasoconstriction and to facilitate the occurrence of seizures from the catecholaminergic effects of cocaine. These findings support the use of calcium channel blockers as a strategy to minimize the neurotoxic effects of cocaine."
Maybe finding something that stimulates Ca(2+) increase like cocaine but that doesn't permeate the blood brain barrier would have height increasing effects.
"the Rhod2-Ca fluorescence was unchanged for ∼15 min, increased slightly, and reached a peak of 4.2 ± 0.7% , which was significantly lower (p < 0.003) than for cocaine"<-So ritalin doesn't increase the Ca in the brain as much as cocaine.
"Methylphenidate, like cocaine, is a dopamine transporter and a norepinephrine transporter inhibitor but differs from cocaine in that it is devoid of local anesthetic actions and does not bind to the serotonin transporter[serotonin has been reported to promote chondrogenesis]. Thus, the differences between cocaine and methylphenidate in the induction of increases [Ca2+]i could be attributable to either the differences in their serotonergic effects or their local anesthetic properties. The fact that lidocaine, which is devoid of catecholamienrgic effects, has similar effects to those of cocaine in increasing [Ca2+]i suggests that it is the local anesthetic and not the serotonergic effects of cocaine that underlie its [Ca2+]i increases"<-So maybe anesthetics applied to the epiphyseal bone marrow could induce chondrogenesis, there are local anesthetics after all.
This study(Long-term effects of short-acting methylphenidate on growth rates of children with attention deficit hyperactivity disorder at Queen Sirikit National Institute of Child Health.) states that Ritalin has a growth stunting effect for 6 months but than growth returns to normal and catch up growth is observed. So maybe dopamine transporter and norepinephrine transporter inhibition reduces growth rate?
Ritalin can already pass the blood brain barrier so if it couldn't increase Ca in the brain it likely can't increase it anywhere else. But it didn't decrease it either and showed a slight increase meaning that ritalin wouldn't affect LSJL, PEMF, or LIPUS induced chondrogenic differentiation like caffeine. It will be worth pursuing to see if local anesthetics can induce chondrogenesis in the epiphyseal bone marrow.
There's an almost universal consensus that ritalin slows down growth rate temporarily.
