PharmacoNutrition Reviewed

Source: Neurobiology of Aging (2007), in press
Article Type: Original Research
Authors: A Bender et al.

Image taken from: http://www.scienceinafrica.co.za/pics/06_2004/brain.jpg

Creatine (an amino acid derivative) is a widely used food supplement due to its putative ergogenic, i.e. exercise capacity enhancing, effect. In terms of exercise performance, a recent review by Paddon-Jones and colleagues (J. Nutr. 134) concludes that creatine is suggested to be of benefit to exercise lasting 30 seconds or less; in contrast, no direct effect of creatine supplementation on muscle protein synthesis has been found. Nonetheless, creatine sales still reached US$ 220 million in 2005.
So whereas creatine might do rather little to improve exercise performance, it still seems to improve health. And not only this, but also survival – at least in mice. Based on previous reports demonstrating protective effects for creatine in models of neurodegeneration, Bender et al. tested the hypothesis whether creatine might also facilitate healthy aging, particularly of the brain, in wild-type mice. In essence, feeding mice a diet containing 1% creatine from 12-month of age onwards, significantly increased both mean and maximum life span in comparison to control mice. Somewhat confirming what was said already above, the creatine-fed mice did not differ in the rotarod and grip strength analyses; however, creatine feeding improved (p<0.05) several markers of memory performance such as object recognition. Also, biomarkers of brain aging due to oxidative stress tended to be lower in the creatine-fed group. Based on gene expression profiling experiments, the authors conclude that creatine not only reversely regulates gene expression altered in aging, but also concordantly affects gene expression as in mice on caloric restriction. Whether this effect of creatine is due to the induction of mild stress like in the case of caloric restriction is unknown. Another potential mechanism of creatine-induced neuroprotection might be the prevention of ROS (recative oxygen species) generation due to enhanced activity of mitochondrial creatine kinase activity, as recently shown by Meyer et al. (JBC 281).
In light of the rather minor safety concerns raised regarding creatine supplementation, it might be worth to further explore the potential of this amino acid derivative to improve healthy aging.

Source: Journal of Neurochemistry (2007), 100: 736-746
Article Type: Original Contribution
Authors: F. Herrera, V. Martin, G. Garcia-Santos, J. Rodriguez-Blanco, I. Antolin, C. Rodriguez

Image taken from:
http://www.virginia.edu/insideuva/2005/11/images/Jet_Lag_Graphic.jpg

Life depends on information. Melatonin, which occurs ubiquitiously in plants and animals, has been suggested as one of the first signals appearing on earth. In vertebrates, it is mainly synthesized in the pineal gland (but also other tissues) from the neurotransmitter serotonin. Melatonin, due to its chronobiotic activity, effectively attenuates jet lag symptoms, especially with eastbound flights. Moreover, melatonin has been shown to prevent neuronal cell death both in vitro and in vivo.
The article by Herrera et al. provides further inside in the mechanism of melatonin-mediated neuroprotection. The authors suggest for melatonin a novel, direct antioxidant effect targeted to the mitochondria, the key source of potentially deleterious reactive oxygen species (ROS) in cells. The protective effects of melatonin in murine hippocampal cells, however, where detected with a melatonin concentration of 1 mM (= 1000 µM), which is in contrast not only to the low micromolar concentrations that have been reported as physiological concentrations of melatonin but also to pharmacological levels, which range between 100 nM-10 µM (Kolar et al.). Bearing in mind these facts, it is somewhat difficult to estimate whether melatonin exerts the aforementioned mode of action in vivo, too.