Michael W. Green

Nutritional influences on cognitive function: mechanisms of susceptibility

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 understanding 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 prevailed. 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 positive 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 interfering 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, glucocorticoid secretion, and pancreatic beta-cell function, rather than simple fuelling 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.

Body iron is associated with cognitive executive planning function in college women.

Evidence of the relationship between altered cognitive function and depleted Fe status is accumulating in women of reproductive age but the degree of Fe deficiency associated with negative neuropsychological outcomes needs to be delineated. Data are limited regarding this relationship in university women in whom optimal cognitive function is critical to academic success. The aim of the present study was to examine the relationship between body Fe, in the absence of Fe-deficiency anaemia, and neuropsychological function in young college women. Healthy, non-anaemic undergraduate women (n 42) provided a blood sample and completed a standardised cognitive test battery consisting of one manual (Tower of London (TOL), a measure of central executive function) and five computerised (Bakan vigilance task, mental rotation, simple reaction time, immediate word recall and two-finger tapping) tasks. Womens body Fe ranged from - 4·2 to 8·1 mg/kg. General linear model ANOVA revealed a significant effect of body Fe on TOL planning time (P= 0·002). Spearmans correlation coefficients showed a significant inverse relationship between body Fe and TOL planning time for move categories 4 (r - 0·39, P= 0·01) and 5 (r - 0·47, P= 0·002). Performance on the computerised cognitive tasks was not affected by body Fe level. These findings suggest that Fe status in the absence of anaemia is positively associated with central executive function in otherwise healthy college women.

Impairments in working memory associated with naturalistic dieting in women: No relationship between task performance and urinary 5-HIAA levels.

The present study investigated the question of whether the previously observed impairments of working memory characteristic of dieting to lose weight can be explained in terms of preoccupying cognitions relating to body shape or to alterations in serotonergic function resulting from a low dietary intake of tryptophan. The population comprised female non-dieting, lower restrained eaters (N=23), non-dieting higher restrained eaters (N=11) and current dieters (N=19). Each participant completed three tasks, each of which selectively loaded on to a different sub-component of working memory. The tasks comprised the Tower of London task, a letter string recall task and a mental rotation task. In addition, all participants completed self-report measures of body shape concern and affective state. Serotonin turnover was assessed by means of 24 h urine sample collection for each participant on their day of testing. This was analysed (via HPLC) for levels of the main serotonin metabolite 5-HIAA.The results of the present study broadly replicated previous findings of a Central Executive and Phonological Loop (but not Visuo-Spatial Sketchpad) deficit in those subjects who reported themselves to be currently dieting. Tower of London task performance also significantly correlated with self-reported feelings of fatness and body shape disparagement. There were no group differences in 5-HIAA levels nor did 5-HIAA levels correlate with task performance. However, there was a significant negative correlation between 5-HIAA levels and self-reported depression. These results support the hypothesis that the variables mediating this deficit are preoccupying cognitions concerning body shape. They do not support the hypothesis that the serotonergic function of dieters is compromised, although this conclusion is tentative.

Weight loss strategies, stress, and cognitive function: Supervised versus unsupervised dieting

The early stages of dieting to lose weight have been associated with neuro-psychological impairments. Previous work has not elucidated whether these impairments are a function solely of unsupported or supported dieting. Raised cortico-steroid levels have been implicated as a possible causal mechanism. Healthy, overweight, pre-menopausal women were randomised to one of three conditions in which they dieted either as part of a commercially available weight loss group, dieted without any group support or acted as non-dieting controls for 8 weeks. Testing occurred at baseline and at 1, 4 and 8 weeks post baseline. During each session, participants completed measures of simple reaction time, motor speed, vigilance, immediate verbal recall, visuo-spatial processing and (at Week 1 only) executive function. Cortisol levels were gathered at the beginning and 30 min into each test session, via saliva samples. Also, food intake was self-recorded prior to each session and fasting body weight and percentage body fat were measured at each session. Participants in the unsupported diet condition displayed poorer vigilance performance (p = 0.001) and impaired executive planning function (p = 0.013) (along with a marginally significant trend for poorer visual recall (p = 0.089)) after 1 week of dieting. No such impairments were observed in the other two groups. In addition, the unsupported dieters experienced a significant rise in salivary cortisol levels after 1 week of dieting (p < 0.001). Both dieting groups lost roughly the same amount of body mass (p = 0.011) over the course of the 8 weeks of dieting, although only the unsupported dieters experienced a significant drop in percentage body fat over the course of dieting (p = 0.016). The precise causal nature of the relationship between stress, cortisol, unsupported dieting and cognitive function is, however, uncertain and should be the focus of further research.

Mood, eating behaviour and attention

BACKGROUND Obesity is a growing health problem, but most people find dieting unsuccessful. Three studies examine possible reasons for the difficulty and the extent to which dieting-related reductions in cognitive function are associated with mood and well-being. METHOD In Study One, 49 female dieters were compared with a control group of 31 matched non-dieters on measures of well-being, mood, eating behaviour (Dutch Eating Behaviour Questionnaire), and attention. Study Two examined two measures of restraint to examine why previous studies find high restrainers are prone to react to emotion. Study Three experimentally manipulated mood using music and the standard Velten Induction Procedure to examine attention in restrainers and emotional eaters. RESULTS Dieting was found to be associated with deficits in sustained attention. This finding was further supported by the demonstration of a significant impairment in performance following a negative mood induction in high emotional eaters whereas high restrainers were relatively unaffected by the mood challenge. CONCLUSIONS We suggest that different aspects of eating behaviour have dissociable effects on cognitive-affective function. Trait tendencies to restrained eating are associated with attentional deficits, but are not further affected by mood disruption. It is the long-term tendency to eat when emotional that combines with current emotional state to trigger cognitive deficits.

Pre-existent expectancy effects in the relationship between caffeine and performance

The present study investigated the impact of pre-existent expectancy regarding the effects of the caffeine load of a drink and the perception of the caffeine content on subjective mood and vigilance performance. Caffeine deprived participants (N=25) were tested in four conditions (within subjects design), using a 2×2 design, with caffeine load and information regarding the caffeine content of the drink. In two sessions, they were given caffeinated coffee and in two were given decaffeinated coffee. Within these two conditions, on one occasion they were given accurate information about the drink and on the other they were given inaccurate information about the drink. Mood and vigilance performance were assessed post ingestion. Caffeine was found to enhance performance, but only when participants were accurately told they were receiving it. When decaffeinated coffee was given, performance was poorer, irrespective of expectancy. However, when caffeine was given, but participants were told it was decaffeinated coffee, performance was as poor as when no caffeine had been administered. There were no easily interpretable effects on mood. The pharmacological effects of caffeine appear to act synergistically with expectancy.

Cognitive Performance Deficits of Dieters

The present chapter reviews the literature concerning the psychological effects of one of the most commonly undertaken food choice-related behaviors in the Developed World– caloric restriction via weight loss dieting. The severe chronic caloric restriction associated with anorexic psychopathology is associated with a range of neuropsychological impairments resulting from starvation-related alterations in brain anatomy and chemistry. Severe, chronic nonpsychopathological caloric restriction has also been associated with a range of impairments in cognitive function and mood. The degree of caloric restriction characteristic of weight loss dieting has, however, been less reliably associated with impaired psychological function, the phenomenon being dependant on the manner in which weight loss is attempted, the degree of weight loss, and the precise nature of the psychological assessment battery. In general, the evidence concerning the effects of controlled, laboratory-based caloric restriction is mixed, with some studies showing no effects of laboratory-induced caloric restriction, some showing a negative psychological impact of restriction, and some actually showing an improvement in certain psychological domains (recognition memory). Methodological issues surrounding this phenomenon are discussed. In contrast, spontaneously undertaken weight loss is reliably associated with impairments in the performance of a range of cognitive performance measures. Primarily, the cognitive deficit associated with spontaneous dieting appears to be a reduction in available working memory capacity, this being the cognitive system which allocates limited cognitive resources to other, ongoing activities and remembering the moment-to-moment rules of action. This reduction results from dieting-related preoccupying cognitions concerning body shape, hunger, and food which preferentially consume the limited amount of working memory capacity. Support for this, rather than a biological explanation, can be seen in the findings that the cognitive impairments are most marked during the early stages of attempted weight loss and are independent of the degree of weight actually lost over the course of the diet.