Risk Factors and Neurocognition

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A host of behavioral, biomedical, psychosocial, and psychophysiological risk factors can influence cognitive performance. Importantly, relations of these risk factors (and diseases) to cognitive outcomes may be moderated by select genotypes. For example, the apolipoprotein E (APOE) e4 allele is associated with AD, cognitive decline (Farrer et al, 1997), cardiovascular disease, and stroke (Eichner et al, 2002). Haan and colleagues (1999) noted that among individuals with cardiovascular and metabolic diseases, those who had an APOE e4 allele experienced a significantly greater rate of cognitive decline than those without.

Numerous lifestyle factors that promote or reduce risk for chronic disease have known a impact on cognitive function and its decline. Various health-compromising behaviors exert a negative influence on cognitive function, whereas health-enhancing behaviors are associated with higher levels of performance or potential improvement with intervention. Lifestyle factors can influence cognitive performance by impacting the brain directly or by promoting or reducing the development of chronic diseases that in turn affect the brain. Examples of health-compromising behaviors that are associated with lower levels of cognitive function include smoking (Swan and Lessov-Schlaggar, 2007), heavy alcohol consumption (Oscar-Berman and Marinkovic, 2007), dietary insufficiencies (Gillette et al, 2007), and physical inactivity (Colcombe et al, 2004). Health-enhancing behaviors such as greater intake of antioxidants including omega-3 fatty acids, and vitamins C and E have been associated with higher levels of cognitive performance (Del Parigi et al, 2006; Morris et al, 2004), although results of randomized clinical trials have been mixed. Greater levels of fitness or physical activity have also been related to better cognitive performance (Colcombe et al, 2004). Further, aerobic exercise has demonstrated exciting associations with cognitive improvements and even neuro-plasticity in both animal models and humans

(Dishman et al, 2006; Lautenschlager et al, 2008).

Various traditional biomedical risk factors for disease and newer biomarkers are associated with lower levels of cognitive function and decline. Examples include high levels of blood pressure (or hypertension; Waldstein and Katzel, 2001), cholesterol (Muldoon et al, 2001), glucose (even in a non-diabetic range; Taylor and MacQueen, 2007), insulin (Stolk et al, 1997), homocysteine (Elias et al, 2005), obesity (Gunstad et al, 2007), pro-inflammatory markers (e.g., interleukin-6; Yaffe et al, 2003), and indices of oxidative stress (Berr et al, 2000). Interestingly, both high and low levels of several of these risk factors (e.g. blood pressure, cholesterol, body mass index, alcohol consumption) have been related to poorer cognitive outcomes (see Waldstein et al, in press).

Various hormones are known to have a direct biological influence on the brain while potentially promoting diseases that affect cognitive function. In that regard, low levels of estrogen and androgens (Sherwin, 2003, 2006) and both low and high levels of thyroid hormones (Smith et al, 2002) have been related to poorer cognitive function. Hormone therapy in post-menopausal women may help prevent cognitive decline (Sherwin, 2003). Numerous studies have revealed associations between higher resting cortisol levels and lowered levels of cognitive performance, particularly on tests of learning and memory (Lupien et al, 2005). It has also been noted that stress-induced cortisol elevations are associated with decreased cognitive performance (Kirschbaum et al, 1996).

The latter findings reflect a larger literature on the negative relations of stress to cognitive performance and brain structure and function, at least in part via aberrations in cortisol (Sapolsky, 1999; McEwen, 2002). Stress-induced blood pressure responses have also been related to lower levels of cognitive function (Waldstein and Katzel, 2005). In addition to stress-related constructs, it is increasingly recognized that a number of psychosocial factors that may confer risk for chronic disease are related to cognitive function (see Waldstein et al, in press). Depression is such a factor that has long been known to have negative relations to brain and cognition. Other psychosocial factors such as hostility and anxiety may confer a negative influence on cognitive function whereas social support - a factor usually associated with better health outcomes - may have a protective relation to cognitive function.

A number of the aforementioned risk factors such as less healthy lifestyles, psychosocial stressors, and an accumulation of biomedical risk factors may, in part, explain associations of low levels of education or socioeconomic status (SES) and race/ethnicity (e.g., African American) to cognitive performance (Waldstein, 2000). Those of lower SES may also be more likely to experience neurotoxic exposures that impact the brain and cognitive function negatively (Morrow et al, 2001) and are less likely to have access to adequate treatment of their medical conditions.

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