My wife who is an ENT surgeon tells me the steroidal nasal sprays have very low systemic conversion (i.e. 1%). Does anyone know why NMN would be any different? Is it the molecule size? Dr David?guest1576 wrote: ↑Tue Jul 23, 2019 11:22 pmStudies in mice show nasal spray is at least 10x more available than capsules. For a general rule, you can say 100 mg a day is a good target. That would be 2 sprays, 4 times a day. We have had several people try 500 mg a day for weeks, with no noticable problems, but can't recommend that high of dose. Best bet is to start at 100 mg a day and increase from there.
I am including NAD+ Nasal Spray into my regime in about 2 weeks so I will be posting very soon after that on what I believe will be significant increased benefits. I’m also looking forward to the instantaneous results after administering the spray.. in conjunction with the NMN..stay tuned
Prevention of Traumatic Brain Injury-Induced Neuron Death by Intranasal Delivery of Nicotinamide Adenine Dinucleotide (won, 2012)
The present study demonstrates that intranasally-administered NAD+ increases hippocampal NAD+ levels and reduces TBI-induced neuronal death in the hippocampus.
Intraperitoneal injection of the same NAD+ concentration that we used for intranasal administration showed no neuroprotective effects on TBI-induced neuronal death.
Compared with NAD+-treated rats, nicotinamide treatment showed no protective effects against TBI-induced neuronal death
Intranasal administration with NAD+ profoundly decreases brain injury in a rat model of transient focal ischemia (ying, 2007)
Increasing evidence has supported the hypothesis that PARP-1 induces cell death by depleting intracellular NAD+. We observed that intranasal NAD+ delivery significantly increased NAD+ contents in the brains. Intranasal delivery with 10 mg / kg NAD+ at 2 hours after ischemic onset profoundly decreased infarct formation when assessed either at 24 or 72 hours after ischemia. The NAD+ administration also significantly attenuated ischemia-induced neurological deficits. In contrast, intranasal administration with 10 mg / kg nicotinamide did not decrease ischemic brain damage. These results provide the first in vivo evidence that NAD+ metabolism is a new target for treating brain ischemia, and that NAD+ administration may be a novel strategy for decreasing brain damage in cerebral ischemia and possibly other PARP-1-associated neurological diseases.
Our results provide the first in vivo evidence that NAD+ administration can profoundly decrease brain damage under certain pathological conditions. It is noteworthy that NAD+ can reduce infarct formation by up to 86 % even when administered at 2 hrs after ischemic onset. Compared with other studies that apply drugs during post-ischemia phases in order for decreasing ischemic brain injury, the protective effect of NAD+ could be one of the most profound effects ever reported. In this study we also provided evidence that by the intranasal delivery approach NAD+ can be delivered into the brains.
Multiple studies have suggested that nicotinamide can decease ischemic brain injury, but at doses higher than 125 mg / kg (19). Our study shows that intranasal administration with nicotinamide at 10 mg / kg can not affect ischemic brain damage, in contrast to the profound protective effects of 10 mg / kg NAD+.