glucose ingestion leads to increased memory performance

Posted comment on ´Sweet Memories` by M.A. Smith and published in the Psychologist 28/3 March 2015


The observation that increased glucose levels under certain conditions can lead to increased memory and cognitive performance (the so-called ´glucose memory facilitation effect`) and conversely the detrimental effect of prolonged high blood glucose in glycaemic dysregulation disorders has been investigated since the 1980s. According to Smith, glucose enhances in an inverted U dose dependent manner and produces the best performance effect with a dose of 25-50g glucose (pure powdered glucose dissolved in water), equivalent to the consumption of a chocolate bar. Early studies eliciting the more robust results were carried out with elderly individuals or individuals with observable memory deficits (Smith, Riby et al, 2011) and therefore, the glucose memory facilitation effect was assumed to occur in individuals not at their ´cognitive peak`, i.e. where cognitive performance could be measurably improved. Most early studies involving verbal episodic memory tests (the encoding and recall of a word list) resulted in the glucose memory facilitation effect being observed, whereas the results of studies measuring other cognitive capabilities appeared ambiguous. Hence, Riby and Riby 2006 suggested that the effect of glucose on memory occurred because of its effect on hippocampal functioning.
In the 1990s and early 2000s, Foster and Sünram-Lea studied the glucose memory facilitation effect in young people who were assumed to be at their ´cognitive peak`. They induced ´room for cognitive improvement` by asking the participants to perform dual tasks (verbal episodic memory performance whilst hand movement sequences were being simultaneously performed). Attention was divided equally on both tasks. The researchers found that episodic memory recall was increased and later experiments using increased task demands also produced the same results. Smith and colleagues also looked at the glucose memory facilitation effect in young healthy adolescents who exhibited ´room for cognitive improvement`. In their research, this condition was created by the participants skipping breakfast after an overnight fast. The participants then ingested a glucose drink or a placebo (using artificial sweetener) and then performed word list learning and immediate or delayed recall tests whilst simultaneously carrying out hand-movement sequences. Under these conditions, the glucose memory facilitation effect was only displayed for delayed recall (20-40mins after ingestion) and only in the case of participants with better glucose regulatory efficiency. A further study using participants exhibiting anxiety produced the same results: those taking the placebo demonstrated poorer verbal episodic memory capacity whereas those who ingested the glucose saw a rise in performance to that of those with lower anxiety levels. Monitoring the rise one week after the ingestion showed that the effect persisted.
Smith and Foster (2008) also investigated the glucose memory facilitation effect by giving participants breakfast meals with either a high or low glycaemic index. As expected they found that with the same dual tasks, those individuals who had ingested the meal with a high glycaemic index demonstrated increased performance. Hence, Smith notes that it appeared that meals with a high glycaemic index were beneficial regarding learning in individuals who were not at their cognitive peak. This introduced a dilemma – advocating high gylcaemic index meals in comparison to low glycaemic index meals for adolescents in order to raise cognitive performance even though such a diet would produce adverse health effects due to the high level of sugar. The health benefits of the low glycaemic index meals were instead advocated by considering the effect on attention where this type of meal leads to improved maintenance of attention with time and hence, improved learning.
Smith describes in his article not only experiments where glucose is administered, but also illnesses where there is prolonged increased blood glucose levels, e.g. Type 2 diabetes. Prolonged increased blood glucose is said to be associated with decreased verbal episodic memory and other cognitive impairments and further studies with older adults found decreased instrumental functional living capacity (e.g. using telephone, managing finances), decreased attention, decreased executive functional tasks, decreased capability of maintaining balance whilst performing cognitive task requiring memory and processing, and an increased number of falls (although this could be directly attributed to diabetes).
The overall conclusion is that the glucose memory facilitation effect can be observed in cases of poorer performance, or when the cognitive demand is increased either by increasing the nature of the task or by dividing attention. In this case there is an observed benefit and this benefit appears to be associated with a longer-term memory effect. Smith associates the glucose memory facilitation effect with activity in the hippocampus, but not wholly selective for this area. The hippocampus is susceptible to the action of insulin and glucose is reported to lead to increased synthesis of neurotransmitters in this area including acetylcholine. It is also said to mediate the regulation of ATP sensitive potassium ion channels leading to neurotransmitter release. Other brain areas are also affected by glucose including the right ventrolateral prefrontal cortex which is involved in verbal episodic memory thus explaining the researchers findings.


On the first cursory reading I and no doubt countless others were uplifted by the thought that just by eating a good breakfast all my memory worries would evaporate. It seemed so simple and so logical – low blood sugar, lower cognitive performance, increase blood sugar, increased cognitive performance. But, and unfortunately there is a ´but`, nothing regarding nature and the human being, is that simple. It is clear that there must be a link between brain functioning and glucose since the main source of cellular energy in the brain is blood glucose, but there are exact mechanisms in place to maintain a continual supply under normal conditions. Blood glucose levels are controlled by the level of insulin and an overnight fast (as used in some of the experiments described above) leads to metabolic changes to counteract the low blood-sugar level resulting from the low dietary intake. Insulin secretion is reduced and there is an increased secretion of glucagon, which is a hormone secreted by the pancreas and signals the liver to breakdown its glycogen stores to glucose-1-phosphate. Hence, glucose levels in the brain may be reduced, but not critical. Anyway, ketone bodies can also be used as a substitute ´fuel`, but this mechanism is employed in longer starvation periods not considered in the experiments described here.
Another aspect of the experimentation given here that needs to be addressed relates to the definition of ´cognitive peak` and those individuals with ´room for improvement`. We are all aware of when we are ´working` well and this could be defined as our ´cognitive peak`. In the experiments described here individuals who would normally be at their ´cognitive peak` are put at a disadvantage by introducing a simultaneous, completely separate, second task. Then, the individual is multi-tasking, employing divided attention tactics to complete the two tasks given. The ability to do this is influenced by many factors including anxiety, the tasks themselves (similarity and difficulty for example) and age and individuals suffering from anxiety and those senior in years were included in the experiments reported in this article. These were given as individuals not at their ´cognitive peak` and other research has shown that in the case of age, the ability to ignore task irrelevant information or distraction is reduced having an impact on processing and learning. Therefore, the experiments described where there was a glucose memory facilitation effect refer to individuals with divided attention due to the performance of dual tasks and other individuals who demonstrate poor performance with regards to divided attention due to inability to disregard irrelevant information.
So, what could explain the positive observations of glucose on memory capability? It is possible that the increased cognitive performance linked to glucose ingestion is caused by a general improvement in neuronal functioning and firing leading to improved attention and concentration for example. This would make it therefore an effect similar to that observed with the administration of caffeine. The glucose memory facilitation effect could be the result of a change in hippocampal functioning as suggested by Smith and there are many links between hippocampal functioning and brain memory. It is known that the hippocampus is required for the recall of information (ie as required for the information of the verbal episodic memory test given) and that learning requires new hippocampal cells, hence the increased glucose concentration (and cellular energy production) may lead to increased or more productive neurogenesis. An increase in neurotransmitter production may also result thus improving cell interaction and neural transmission.
The glucose memory facilitation effect may also be due to increased right ventrolateral prefrontal cortex activity as suggested by Smith. This area is particularly noted for its link to behavioural reversal activity which may indicate an involvement in task switching important in the performance of dual tasks. The lateral prefrontal cortex is also known as the locus of interference for divided attention and hence, since the experiments involve a dual task scenario then a change in activity in this area may affect overall performance.
Another factor that should be considered is the effect that glucose availability might have on serotonin in the brain. In the low post-absorptive period which would equate to ´breakfast-time` after an overnight fast the hypothalamus acts by releasing hormones to motivate the individual to eat in order to maintain the body`s fat reserve and this leads to an increased anticipation of food. The intake of high carbohydrate results in a better intake of tryptophan into the brain because in normal dietary intake tryptophan would have to compete with other molecules for the brain uptake transporters. In the case of high carbohydrate ingestion, there is little competition and hence tryptophan levels in the brain would be high. Since tryptophan is the building block of serotonin, serotonin levels in the brain would increase under these conditions and serotonin is known to have multiple effects on brain functioning and hence, on cognitive performance. For example serotonin is linked to firing of particular brain areas. In the prefrontal cortex there is a link between the level of task relevant material and firing activity. Firing due to serotonergic binding to specific receptors or on the serotonergic effect on dopamine release causes changes in area activity that could explain the increased level of cognitive performance observed.
Therefore, the temporary positive effect of glucose ingestion on memory performance can be explained by a facilitation of firing in several brain areas including the hippocampus and prefrontal cortex both of which would have an effect on learning (hippocampus, long-term memory formation) and dual task performance (attention and task switching). Unfortunately, the glucose effect can only be observed in certain situations and therefore glucose ingestion cannot be described as a panacea for everybody`s memory problems. It does however, provide an aspect of lifestyle that can be easily examined and changed if the situation demands.

And since we`re talking about the topic…………

….since the original research by Scholey in 2001 saw an effect of glucose and oxygen on cognitive performance, should we go back and look at how oxygen has an effect on cognitive performance?

….can we assume that if the dual tasks were not physical (i.e. hand movements) and mental (i.e. verbal episodic learning and recall), but both mental the glucose memory facilitation effect would be even less since multitasking performance is influenced by task similarity and difficulty?

…..would the administration of anti-depressants that increase the level of serotonin remove the effect of the glucose ingestion if the reason for the latter is the increase in the level of brain serotonin?

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