Nutritional Influences on Cognitive Function

Nutrition Research Reviews (2002), 15, 169–206 DOI: 10.1079/NRR200131 © The Authors 2002 Nutritional influences on cognitive function: mechanisms of susceptibility E. Leigh Gibson1* and Michael W. Green2 1Cancer Research UK Health Behaviour Unit, Department of Epidemiology and Public Health, Royal Free and University College Medical School, University College London, 2–16 Torrington Place, London WC1E 6BT, UK 2School of Life and Health Sciences, Aston University, Aston Triangle, Birmingham, B4 7ET, UK The impact of nutritional variation, within populations not overtly malnourished, on cognitive function and arousal is considered. The emphasis is on susceptibility to acute effects of meals and glucose loads, and chronic effects of dieting, on mental performance, and effects of cholesterol and vitamin levels on cognitive impairment. New developments in understand- ing dietary influences on neurohormonal systems, and their implications for cognition and affect, allow reinterpretation of both earlier and recent findings. Evidence for a detrimental effect of omitting a meal on cognitive performance remains equivocal: from the outset, idiosyncrasy has pre- vailed. Yet, for young and nutritionally vulnerable children, breakfast is more likely to benefit than hinder performance. For nutrient composition, despite inconsistencies, some cautious predictions can be made. Acutely, carbohydrate-rich–protein-poor meals can be sedating and anxiolytic; by comparison, protein-rich meals may be arousing, improving reaction time but also increasing unfocused vigilance. Fat-rich meals can lead to a decline in alertness, especially where they differ from habitual fat intake. These acute effects may vary with time of day and nutritional status. Chronically, protein-rich diets have been associated with decreased posi- tive and increased negative affect relative to carbohydrate-rich diets. Probable mechanisms include diet-induced changes in monoamine, especially serotoninergic neurotransmitter activity, and functioning of the hypothalamic pituitary adrenal axis. Effects are interpreted in the context of individual traits and susceptibility to challenging, even stressful, tests of performance. Preoccupation with dieting may impair cognition by interfer- ing with working memory capacity, independently of nutritional status. The change in cognitive performance after administration of glucose, and other foods, may depend on the level of sympathetic activation, glucocor- ticoid secretion, and pancreatic ␤-cell function, rather than simple fuelling Abbreviations: CCK, cholecystokinin; IQ, intelligence quotient; LNAA, large neutral amino acids; MFF, Matching Familiar Figure; TRP, tryptophan; TYR, tyrosine; 5-HT, serotonin. *Corresponding author: Dr E. L. Gibson, fax +44 20 7813 2848, email [email protected] Downloaded from https://www.cambridge.org/core. IP address: 170.106.33.22, on 25 Sep 2021 at 12:47:16, subject to the Cambridge Core terms of use, available at https://www.cambridge.org/core/terms. https://doi.org/10.1079/NRR200131 170 E. L. Gibson and M. W. Green of neural activity. Thus, outcomes can be predicted by vulnerability in coping with stressful challenges, interacting with nutritional history and neuroendocrine status. Functioning of such systems may be susceptible to dietary influences on neural membrane fluidity, and vitamin-dependent cerebrovascular health, with cognitive vulnerability increasing with age. Glucose: Cognition: Cortisol: Memory: Stress Introduction The present review is concerned with interpreting the somewhat inconsistent findings from research into effects of food and nutrients on cognitive function. Can patterns be discerned that allow better prediction of responses to nutritional changes, based on knowledge of individual characteristics? Could research findings in this area be better understood as interactions between affective state and cognitive function? The view is taken that assessment of cognitive function involves challenging, even stressful, tasks, on which performance may both elicit and depend on changes in affective state and stress responses. This conceptualisation allows nutritional effects on cognitive function to be mediated by changes in affect or arousal as well as or instead of direct effects on perception, attention and memory. Furthermore, it is argued that more emphasis should be given to both inter- and intra-individual differences in nutritional, arousal and stress-coping status, since these may reflect variation in susceptibility of neurohormonal systems to nutritional manipulation. Nutritional variation v. malnutrition Chronic malnutrition undoubtedly hinders cognitive development and performance (Kretchmer et al. 1996; Dauncey & Bicknell, 1999). However, the present review is not concerned with that literature, nor with the pharmacological effects of ingested substances such as caffeine or alco- hol (Rogers, 1995; Bellisle et al. 1998); instead, we review the evidence that acute variation in nutritional status, such as through omission of a meal or by eating a meal of particular composition, may influence cognitive performance or arousal. The impact of variation in nutritional indicators such as blood glucose or vitamins is also included, where these may be considered as measures of nutritional status among populations not overtly malnourished. The susceptibility of cognitive function to such variation may depend on other factors, such as age and vulnerability to stress. Impact of meals on mental function and arousal ‘…fits of drowsiness are especially apt to come on after meals’Aristotle (350 BC) ‘On Sleep and Sleeplessness’ (translated by J. I. Beare) The postprandial period has long been associated with a restful, quiescent state (Hutchinson, 1952); indeed, in many cultures, a post-lunch nap or ‘siesta’ is built into the society’s daily rhythm. Conversely, hunger has been associated with activation and arousal, poor attention, irritability and aggression (Carlson, 1916; Laessle et al. 1996; Kleinman et al. 1998). Downloaded from https://www.cambridge.org/core. IP address: 170.106.33.22, on 25 Sep 2021 at 12:47:16, subject to the Cambridge Core terms of use, available at https://www.cambridge.org/core/terms. https://doi.org/10.1079/NRR200131 Nutritional effects on cognition 171 So, are we more alert and mentally efficient, or over-aroused, distracted and less efficient, before eating than after? It is well established that sympathoadrenal arousal enhances memory formation (McGaugh, 1989). Yet, although eating might be considered to be the antithesis of a ‘flight or fight’ state of arousal, it has been recognised for some time that food ingestion causes an acute rise in sympathetic nervous system output, resulting, for instance, in an increase in car- diac activity (Young & Landsberg, 1977; Vaz et al. 1995; Biston et al. 1996). Thus, eating and arousal are not simple opposites. Indeed, eating a meal, or at least its post-ingestive conse- quence, is a substantial challenge to the body’s homeostasis, and in that sense has been viewed as a stressor (Woods, 1991). However, whereas most stressors are potentially harmful, leading to stress responses designed to avoid or minimise their effects, ingestion and absorption of nutrients are, normally, of benefit, and often essential, to the organism. Nevertheless, the body needs to prepare and react appropriately to this sudden influx of nutrients, if their absorption and use are to be optimal, and minimally disruptive. As our eating habits become established, the brain and body become tuned for rapid and appropriate preparation, based on anticipation of meal composition and after-effects, through early detection of sensory and nutritional prop- erties (Woods & Strubbe, 1994; Teff, 1996). It is within this context that acute nutritional influences on cognitive function and arousal need to be considered. First, we address evidence for the importance of meal timing during the day, dealing with studies of overall meal effects, in the context of circadian rhythms. Then we consider the influences of the size and composition of meals, in particular where findings suggest mechanisms of susceptibility. The importance of meal timing In man, as in many other animals, there are circadian rhythms and sleep–wake cycles in arousal and performance, which complicate interpretation of the impact of meals. Why should a ‘siesta’ be needed after lunch, but not after breakfast or an evening meal? Whereas there are many examples of a decline in feelings of vigour and increases in sleepiness in the hours after a midday meal (Lieberman et al. 1986; Smith & Kendrick, 1992; Owens et al. 2000), it is often not clear whether this is due to eating a meal or merely the time of day. Folkard & Monk (1985) concluded that this ‘post-lunch dip’ in performance or arousal probably has both endogenous and exogenous components; when subjects were isolated from time cues, diurnal deterioration in performance similar to the post-lunch dip was seen, but independently of meal timing. Self-reported alertness or energy rises to a peak in the late morning or midday, then falls later in the waking day (De Castro, 1987a; Smith, 1992). Circadian changes in alertness have often been linked to changes in core body temperature, considered a correlate of physiological arousal (Folkard & Monk, 1985; Owens et al. 2000). Yet, in rats at least, there are clear preprandial rises and postprandial falls in core temperature (Woods & Strubbe, 1994); such meal-dependent changes in body temperature do not appear

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