roscientists) presented their findings and experiences on various TBI-related topics, with a focus on potential nutrient interactions with the pathogenic sequelae of TBI. The committee also reviewed the existing literature examining the pathology and metabolic alterations of the insult with the goal of identifying nutrients that had the potential to favorably alter metabolism, oxidative stress, and tissue structure and repair, following and sometimes in advance of TBI.
As a background to elucidate the committee’s rationale, a summary of current knowledge about the pathophysiology of TBI was presented in Chapter 3. Briefly, brain injuries differ dramatically from patient to patient depending upon the location, type, intensity, and duration of the initiating concussion force. One common feature of severe brain injury is reduced blood flow and oxygen deficiency. Neuronal membranes become damaged and ion channels malfunction, leaking proteins and neurotransmitters. Apoptotic genes are activated, brain cells begin to swell, and mitochondrial function diminishes as the brain cells enter a “death spiral” (Scudellari, 2010). Production of free radicals increases and calcium ions are released, resulting in tissue damage and cell death (Mattson and Chan, 2003). For the purposes of this report, TBI pathology has been divided into primary, secondary, and long-term injury mechanisms to permit more specific focus on the timing and locus of the nutrient intervention. Box 4-1 shows a summary listing of adverse physiological responses as well as select potential neuroprotective targets (e.g., control of inflammation, angiogenic and neurogenic repair and recovery) discussed during the June public workshop and committee meetings that might respond to nutritional interventions. Box entries with an asterisk indicate especially promising potential targets for nutritional intervention. These potential nutritional targets and the mechanism or metabolic bridge linking them to TBI treatment or prevention have been grouped into three topic areas and will be discussed briefly in this chapter. Table 4-1 matches these potential nutritional targets with nutrients having relevant mechanisms of action; however, the reader should make no conclusions about the clinical efficacy of any of these nutrients based on this table. The information in this table is not meant to imply that there is any evidence from animal models or human trials showing benefits in ameliorating TBI. The table was constructed to illustrate that those nutrients and food components act on multiple and diverse processes that are common to brain injury, and therefore their effects (beneficial and adverse) should be reviewed.
For most nutrients, more than one mechanism is proposed. The scientific community believes that, based on the variations in injuries, responses, and outcomes after TBI, no single nutritional mechanism will serve as the magic bullet for TBI. The evidence on the ability of these putative nutrients to improve resilience or ameliorate the effects of TBI will be discussed in detail in subsequent chapters (Chapters 6–16).
From its discussions, the committee identified an initial list of search criteria and promising pre- and postinjury nutritional interventions that might be useful adjuncts in the overall medical treatment and prevention of TBI. The committee decided on the search criteria and vocabulary included in Box 4-2.