She recruited 31 men* and asked them to sniff either an oxytocin nasal spray or another spray with the same ingredients minus oxytocin – a placebo. A few weeks later, the sprays were swapped so that the men who took oxytocin now took the placebo, and vice versa. At the time, neither the scientists nor the volunteers knew which was which – that was only revealed after the experiment was over.

PDGF-BB (Mustoe et al., 1994), FGF-2 (Inadomi et al., 2004), IGF I and II (Zhao et al., 1995), TGF-β (Greenalgh, 1996), and L-arginine (Shi et al., 2003) enhance fibroblast proliferation and deposition of collagen in chronic wounds. Thymosin β4 accelerates wound repair in both young and old diabetic mice by significantly increasing wound contraction and collagen deposition. A synthetic peptide that duplicated the actin-binding domain of thymosin β4 promoted wound repair in aged mice to a degree comparable to that of the whole molecule (Philp et al., 2003). In rats with wound healing impaired by mitomycin C, the formation of granulation tissue (angiogenesis and fibroblast proliferation) was significantly advanced by hydrogel sheets composed of alginate, chitin/chitosan, and fucoidin (Murakami et al., 2010).
In a study measuring oxytocin serum levels in women before and after sexual stimulation, the author suggests it serves an important role in sexual arousal. This study found genital tract stimulation resulted in increased oxytocin immediately after orgasm.[105] Another study reported increases of oxytocin during sexual arousal could be in response to nipple/areola, genital, and/or genital tract stimulation as confirmed in other mammals.[106] Murphy et al. (1987), studying men, found oxytocin levels were raised throughout sexual arousal with no acute increase at orgasm.[107] A more recent study of men found an increase in plasma oxytocin immediately after orgasm, but only in a portion of their sample that did not reach statistical significance. The authors noted these changes "may simply reflect contractile properties on reproductive tissue".[108]
The short half-life (<2h)[16] of 5-HTP may inherently limit the therapeutic potential of 5-HTP,[17] as the systemic 5-HTP exposure levels will fluctuate substantially, even with relatively frequent dosing. Such exposure fluctuations are usually associated with increased adverse event burden, resulting from Cmax drug spikes, and decreased clinical efficacy resulting from sub-therapeutic exposure for large parts of the day. It has been proposed that 5-HTP dosage forms achieving prolonged delivery would be more effective,[17] as is generally the situation with short-acting active pharmaceutical ingredients.[18]
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