and as either dietary supplements or as a component of foods. The committee selected flavonoids as a group of compounds, and curcumin (a flavonoid) and resveratrol (a stilbene) as single components. Although none of these compounds has been tested in human trials, the positive findings from animal models of TBI indicate that resveratrol and curcumin warrant more research to study their effects both in providing resilience to and in treatment of TBI.
The role of vitamin D in the brain has only recently been recognized and is not well understood. Vitamin D and its receptor are thought to act by binding to DNA response elements that regulate gene transcription involved in cell proliferation, differentiation, and neural function in the brain.
Trials to evaluate the effects of progesterone in animal models of TBI have revealed that adequate vitamin D status might affect the outcomes of progesterone treatment, an example of the synergistic effects that may result from interactions among compounds. Vitamin D’s potential to increase resilience to TBI is supported by findings that vitamin D alone was also neuroprotective against animal models of stroke. Although there are only a few studies on vitamin D’s benefits for TBI treatment, the findings are promising and need to be evaluated further.
Zinc is an essential nutrient required for the function of many enzymes in the central nervous system. In the brain, zinc is released in the synaptic cleft where it modulates the activity of neuroreceptors. An excessive release of zinc can result in neural cell death. In the context of TBI, zinc deficiency might exacerbate the oxidative cascade that results in cell death. The nutrition assessments of TBI patients recommended here will help substantiate the hypothesis that zinc deficiency affects outcomes of TBI. Findings from animal studies suggest that supplementation of diets beyond required levels might be even more beneficial, and this possibility should be explored. Trials of patients with severe closed head injuries showed positive effects after treatment with zinc.
Ultimately, interventions for which there is sufficient evidence of efficacy need to be transferred to clinical care situations. In general, the majority of clinical guidelines for critical care and for TBI do not include specific recommendations to ensure adequate nutrition early after injury or in the long term. The findings of the research gaps outlined above would present an opportunity to update the existing clinical guidelines with evidence-based nutritional interventions.
DoD (Department of Defense). 2009. Traumatic brain injury care in the Department of Defense. http://www.dcoe.health.mil/Content/Navigation/Documents/Traumatic%20Brain%20Injury%20Care%20in%20the%20Department%20of%20Defense.pdf (accessed January 14, 2011).
Masel, B. E., and D. S. DeWitt. 2010. Traumatic brain injury: A disease process, not an event. Journal of Neurotrauma 27(8):1529–1540.