(2004) demonstrated that cortical and hippocampal levels of lactate and free fatty acids are lower in rats fed creatine than in nonsupplemented rats (Scheff and Dhillon, 2004). These results provide support for the hypothesis that creatine’s neuroprotective effects are at least partly due to a reduction in the processes associated with secondary brain damage.
It also has been proposed that the neuroprotective effects of creatine may reflect its ability to improve cerebrovascular function (Prass et al., 2007). Support for this proposal comes from a recent study demonstrating that feeding creatine to mice subjected to middle artery occlusion resulted in reductions in infarct volumes. Although there were no changes in brain creatine, phosphocreatine, ATP, ADP, or adenosine monophosphate (AMP), such supplementation did improve cerebral blood flow in these animals, suggesting that creatine may have beneficial effects on cerebrovascular functioning.
A list of human studies (years 1990 and beyond) evaluating the effectiveness of creatine in providing resilience or treating TBI or related diseases or conditions (i.e., subarachnoid hemorrhage, intracranial aneurysm, stroke, anoxic or hypoxic ischemia, epilepsy) in humans is presented in Table 10-1. This also includes supporting evidence from animal models of TBI. Although this report does not generally include studies on the effectiveness of nutrition interventions on long-term effects of TBI effects, depression as an effect of TBI has been included in this chapter. The occurrence or absence of adverse effects in human studies is included if reported by the authors.
Creatine is one of the most widely used dietary supplements. Athletes, body builders, and military personnel use creatine to enhance muscle mass and increase strength. Creatine is also used as an ergogenic aid to improve performance of high-intensity exercise of short duration (Bemben and Lamont, 2005; Branch, 2003; IOM, 2008). Creatine’s popularity as a dietary supplement was further increased by a 2006 study demonstrating its positive effect on cognitive and psychomotor performance (McMorris et al., 2006).
Because it can be synthesized in the body, there is no Recommended Dietary Allowance for creatine; however, as a result of daily losses, creatine stores need to be maintained either by diet or synthesis. Research indicates that creatine supplementation increases the creatine and phosphocreatine pools in muscle, particularly in younger individuals who are engaging in vigorous physical activity, and in vegetarians, who may have a less than optimal pool of phosphocreatine (Brosnan and Brosnan, 2007; Burke et al., 2003; Rawson et al., 2002).
Experiments among athletes and military personnel indicate that creatine taken at levels commonly available in supplements produces minimal, if any, side effects (IOM, 2008; Shao and Hathcock, 2006). Using evidence from well-designed, randomized controlled human clinical trials of creatine, Shao and Hathcock (2006) concluded that chronic intake of 5 g/day of creatine was safe and posed no significant health risks.
As with other nutrients or food components, the committee found no human studies testing the potential benefits of creatine in TBI or other related diseases or conditions included in the reviewed of the literature (subarachnoid hemorrhage, intracranial aneurysm, stroke, anoxic or hypoxic ischemia, epilepsy).