Glucose Mood and Mental Function

The possibility that ingesting glucose can alter mood and improve mental function has generated considerable research interest. However, there is space here only to summarize and interpret the key findings and controversies. The interest in glucose arises from two observations: first, that the primary source of energy for brain function is glucose, and, second, that mental function and mood deteriorate when blood glucose concentration falls below basal physiological levels (hypoglycemia; <3.6 mmol l_1). The first observation must be qualified by recent evidence that, first, in times of metabolic demand, the brain can also use lactate very effectively as an energy source, and, second, the brain contains significant stores of glycogen in specialized cells called astrocytes, which can be metabolized for energy by neighboring neurones. Nevertheless, in rats, extracellular glucose levels in a specific region of the brain critical for memory, the hippocampus, decline to a greater extent during more demanding memory tasks, and this decline is prevented by a systemic glucose load.

Hypoglycemia is rarely induced by normal food, although large quantities of sugar-rich drinks taken on an empty stomach might do so in some people. Yet, many studies of the effects of glucose use a method similar to the oral glucose tolerance test

(OGTT), in which fasted patients drink aqueous solutions containing 50-75 g of some form of glucose. This is meant to be not a normal nutritional manipulation but a test of glucoregulation. Associations have been reported between rapid and substantial declines in blood glucose after OGTTs and aggressive thoughts and behavior. However, this might be mediated by greater counter-regulatory hormone release.

In studies comparing sugar-rich drinks with zero-energy sweet placebos, many participants report no effect on mood, but some report a rise in subjective energy within an hour, followed by increased calmness. In children, controlled studies failed to support the popular myth that sugar is excitatory: again, it either had no effect or was calming. However, it is worth noting that some adults, and probably children, are especially sensitive to rapid drops in blood glucose, showing counter-regulatory hormone release and 'hypoglycemic symptoms' even though actual hypoglycemic levels of glucose are not reached.

It may be that beneficial effects of glucose ingestion become consistently apparent only when demands are placed on mental function. The findings on glucose and cognitive performance can be summarized as follows.

• The majority of studies that administered a glucose drink found subsequent improvements in performance compared with administration of a placebo, particularly in tests of short-term memory or vigilance tasks that require a large component of 'working memory'.

• Improvements in performance can be associated with rising or falling blood glucose levels, even independently of consuming a glucose load.

• Young healthy subjects require more demanding tasks than the elderly to detect a beneficial effect of glucose load.

• Associations between performance and glucose may be mediated by individual glucoregulatory efficiency.

• Both glucoregulation and performance are influenced by hormones, such as adrenaline and cortisol, that are sensitive to stressful or arousing cognitive tasks.

• Personality, stress-sensitivity, and task involvement can influence glucose uptake and disposal and, hence, the effects of glucose on cognition.

However, one important pattern does emerge: memory performance is worse in poorer than in better glucoregulators (Figure 3). This is true not just for elderly patients but also among a healthy student population, especially if the task is sufficiently demanding. High peak blood glucose predicts poor memory performance in elderly patients, whether or

Time (min)

Figure 3 A model of changes in blood glucose levels after a glucose load in people who are either good regulators (solid line) or poor regulators (broken line) of blood glucose. The increased peak and delayed recovery of blood glucose levels in poor regulators suggests glucose intolerance and insulin resistance. In such people, there may be a brief period of mild hypoglycemia prior to a return to baseline levels. This difference in glucoregulation has been demonstrated in both young and elderly people without diabetes. Poor glucoregulation predicts poor cognitive performance in challenging tests, especially those involving memory.

Time (min)

Figure 3 A model of changes in blood glucose levels after a glucose load in people who are either good regulators (solid line) or poor regulators (broken line) of blood glucose. The increased peak and delayed recovery of blood glucose levels in poor regulators suggests glucose intolerance and insulin resistance. In such people, there may be a brief period of mild hypoglycemia prior to a return to baseline levels. This difference in glucoregulation has been demonstrated in both young and elderly people without diabetes. Poor glucoregulation predicts poor cognitive performance in challenging tests, especially those involving memory.

not a glucose load has been given prior to testing. This relationship between raised glucose levels and poor memory performance could underlie a recent finding that a snack with a high glycemic index (greater plasma glucose rise) resulted in poorer memory performance 2-3 h later than a snack with a low glycemic index. Even so, it seems that a glucose load can lessen the memory deficit present in young and old poor glucoregulators (with little consistency or no effect in good glucoregulators).

One reason why poor glucoregulation predicts poor memory performance may be that glucose intolerance is associated with higher basal and stress-induced cortisol secretion. Cortisol is known to impair memory, probably by an action on hippocampal neurones that includes inhibition of glucose uptake. However, the substantial rise in insulin induced by a glucose load in poor glucoregulators may overcome the negative impact of cortisol in some cases: hyperinsulinemia induced independently of hyperglycemia has been shown to ameliorate memory deficits in patients with Alzheimer-type dementia.

Two other mechanisms might explain the ability of a glucose load to improve performance in subsequent challenging tasks. One is an increase in sympathetic activation by the glucose load: adrenaline is known to enhance memory. The other is increased synthesis and release of the neurotransmitter acetylcholine during challenging tasks: acetylcholine is known to be critically involved in learning and memory and is synthesized from dietary choline and from acetyl CoA, which is a by-product of glucose metabolism.

Diabetes 2

Diabetes 2

Diabetes is a disease that affects the way your body uses food. Normally, your body converts sugars, starches and other foods into a form of sugar called glucose. Your body uses glucose for fuel. The cells receive the glucose through the bloodstream. They then use insulin a hormone made by the pancreas to absorb the glucose, convert it into energy, and either use it or store it for later use. Learn more...

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