There is increasing evidence that sugar, glucose specifically, can influence central nervous system activity. Although memory enhancement was not demonstrated in any of the challenge studies which measured memory in children, there is evidence that glucose levels influence memory functioning in rats and humans, locomotor activity and sleep patterns in rats, and the distress associated with painful procedures in human infants. The focus of research in this area has been to establish how glucose acts to mediate these effects.

Since the retention of memory is an important central nervous system function in the process of cognition, central nervous system mechanisms salient to this function such as noradrenergic and cholinergic systems have been investigated. To investigate the positive effects of epinephrine on memory processing, one study systematically examined the effects of glucose on both animal and human subjects. The study (206) employed a foot shock avoidance task on rats, and observed, similar to the epinephrine effects, significantly improved retention in animals who received 10 to 100 mg/kg injection of glucose immediately after training. No effect was observed if the injection was delayed by one hour or if higher or lower doses were used. In a subsequent study (207), glucose was shown to have similar effects to other memory modulators in that its administration with low foot shock training enhanced the rats’ memory storage while its administration with high foot shock training impaired retention possibly due to endogenous levels of epinephrine produced by the foot shock.

Extending the postulate that glucose improves memory functioning to a human population, one study (208) demonstrated significantly improved memory processing via a standardized measure in nine of eleven elderly human subjects after administration of oral glucose versus placebo. Further, a study found that enhancement of memory in elderly humans twenty-four hours after learning was significantly improved by glucose administration before or after the learning task (209). This may be similar to the finding in rats where memory potentiation in elderly rats was more marked than that demonstrated in a young adult rat population (210). None of the studies of sugar in children showed any effect on memory while those completed with elderly subjects did. However, it is important to note that most of the child studies used sucrose and only a few of them specifically tested memory.

In summary, there is evidence that glucose is discretely involved in neuroendocrine modulation of memory storage in both rats and humans. This influence is best demonstrated in elderly subjects. Further, one site of action of glucose is the medial septum which is rich with communications to the hippocampus. Although, the precise mechanism of the effects of glucose on memory are not yet established, these findings may have far reaching implications for pharmacologic treatment of memory impairments resulting from old age or head trauma. As of now the clinical implications of these findings have yet to be defined. Much more extensive research is required before any conclusions about clinically relevant implications can be drawn.

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