Meal Composition

Carbohydrate versus protein The effects of varying the nutrient composition of meals have been studied extensively, rather more for mood than performance. This is largely because of evidence that plasma and brain levels of precursor amino-acids for the synthesis of monoamine neurotransmitters (chemicals responsible for signalling between nerve cells), strongly implicated in mood disorders, can depend on the ratio between carbohydrate and protein in the diet. Synthesis of the neurotransmitter serotonin (or 5-hydroxytryptamine (5-HT)) depends on the dietary availability of the precursor essential amino-acid, tryptophan, owing to a lack of saturation of the rate-limiting enzyme, tryptophan hydroxylase, which converts tryptophan to 5-hydroxytryptophan (see Figure 1). An important complication is that fpF^ LNAA WW

fpF^ LNAA WW

Blood

Neurone

Neurone

Figure 1 The pathways involved in the synthesis of the neurotransmitter 5-hydroxytryptamine (5-HT; serotonin) from the precursor essential amino-acid, tryptophan (TRP). Tryptophan is taken up by neurones from the blood, but its passage across the blood-brain barrier (BBB) is in competition with that of another group of essential amino-acids known as the large neutral amino-acids (LNAA). Thus, the ratio of tryptophan to total LNAA determines how much tryptophan enters the brain. Most tryptophan is normally bound to albumin in plasma, so it is not available for uptake into the brain. However, after a carbohydrate-rich low-protein meal, increased release of insulin raises levels of free fatty acids (FFA) in plasma, and these displace tryptophan from albumin. In addition, insulin promotes tissue uptake of the LNAA from plasma. Hence, the ratio of tryptophan to total LNAA increases and more tryptophan enters the brain. Increased availability of tryptophan in neurones drives greater synthesis of 5-HT because the rate-limiting enzyme, tryptophan hydroxylase, which converts tryptophan to the intermediate 5-hydroxytryptophan (5-HTP), is not fully saturated.

tryptophan competes with several other amino-acids, the large neutral, primarily branched-chain, amino-acids (LNAA), for the same transport system from blood to brain. If the protein content of a meal is sufficiently low, for example less than 5% of the total energy as protein, then relatively few amino-acids will be absorbed from the food in the gut. At the same time, insulin will stimulate tissue uptake of competing amino-acids from the circulation, and the plasma ratio of tryptophan to those amino-acids (tryptophan/LNAA) will rise, favoring more tryptophan entry to the brain. Conversely, a high-protein meal, which would be less insulinogenic, results in the absorption of large amounts of competing amino-acids into the blood, especially the branched-chain amino-acids (leucine, isoleucine, and valine). On the other hand, tryptophan is scarce in most protein sources and is readily metabolized on passage through the liver: thus, the plasma ratio of trypto-phan to competing amino-acids falls after a protein-rich meal. Indeed, the protein-induced reduction in plasma tryptophan ratio often seems to be more marked than any carbohydrate-induced rise. Such effects also depend on the interval since, and nutrient content of, the last meal.

This evidence is particularly relevant to dietary effects on mood and arousal, because 5-HT has long been implicated in sleep and in affective disorders such as depression and anxiety. However, cognitive performance might also be affected, given the known role of 5-HT in responsiveness to environmental stimuli and stressors, impulsivity, and information processing. Importantly, there is evidence that the dietary availability of tryptophan can influence brain function in humans: for instance, feeding a tryptophan-free diet, which considerably reduced plasma tryptophan (and so could be expected to impair 5-HT function), induced depression in previously recovered depressives and in people with a genetic predisposition to depression. Furthermore, a tryptophan-free drink has been shown to impair performance in tests of visuospatial and visual-discrimination learning and memory.

There is evidence that people feel calmer and sleepier after snacks or meals rich in carbohydrate but virtually free of protein (an unusual situation) than after protein-rich meals containing little carbohydrate. This is compatible with changes in 5-HT function, but these studies did not determine whether this is due to an increase in 5-HT after the carbohydrate-rich meal or a decrease after the protein-rich meal, which could prevent the postprandial sleepiness. Furthermore, adding more than 5-6% protein (of total energy) to the carbohydrate meal has been shown to prevent the increased synthesis of central

No food Carbohydrate 6% Protein 12% Protein 24% Protein 40% Protein only

Meal content

Figure 2 The effect in rats of no meal, a carbohydrate meal with no protein, and meals with increasing amounts of protein on the plasma ratio of tryptophan to the large neutral amino-acids with which tryptophan competes for entry across the blood-brain barrier (cross-hatched bars), levels of tryptophan in the hypothalamus of the rat brain (hatched bars, expressed in mmolg"1), and levels of 5-hydroxytryptophan, an intermediate precursor of serotonin synthesis, in the hypothalamus (open bars, expressed in 0.1 mgg"1)-The rise in tryptophan entering the brain after a carbohydrate meal drives increased serotonin synthesis, but this effect is progressively inhibited by increasing protein content.

No food Carbohydrate 6% Protein 12% Protein 24% Protein 40% Protein only

Meal content

Figure 2 The effect in rats of no meal, a carbohydrate meal with no protein, and meals with increasing amounts of protein on the plasma ratio of tryptophan to the large neutral amino-acids with which tryptophan competes for entry across the blood-brain barrier (cross-hatched bars), levels of tryptophan in the hypothalamus of the rat brain (hatched bars, expressed in mmolg"1), and levels of 5-hydroxytryptophan, an intermediate precursor of serotonin synthesis, in the hypothalamus (open bars, expressed in 0.1 mgg"1)-The rise in tryptophan entering the brain after a carbohydrate meal drives increased serotonin synthesis, but this effect is progressively inhibited by increasing protein content.

5-HT, relative to fasted levels, in both rats and people (see Figure 2). Also, even pure carbohydrate does not appear to induce sleepiness in everyone.

Another difficulty in comparing the effects of carbohydrate and protein intakes is that relative changes in mood and performance might be due to a protein-induced increase in plasma tyrosine, the precursor amino-acid for synthesis of the catechol-amine neurotransmitters (adrenaline, noradrenaline, dopamine), which also competes with LNAA for entry into the brain. In catecholamine systems where the neurones are firing rapidly, acute physiological increases in brain tyrosine (e.g., by feeding a high-protein diet) can raise the tyrosine hydroxyla-tion rate and catecholamine turnover. Such systems include dopaminergic neurones involved in arousal, attention, and motivation. Nevertheless, high-protein meals in humans do not always raise the plasma tyrosine-LNAA ratio; the effect depends on nutritional status and time of day, for example.

Differential effects on performance have been seen with less extreme variations in protein and carbohydrate intakes. For example, a lunch of 55% energy as protein and 15% as carbohydrate produced faster responses to peripheral stimuli, but greater susceptibility to distraction, than eating the reverse proportions of protein and carbohydrate. Sleepiness was not affected by macronutrient composition in that study. However, with these protein-carbohydrate ratios, the plasma tryptophan-LNAA ratio could still be lowered by the protein-rich meal relative to the ratio after the carbohydrate-rich meal, even if tryptophan/LNAA does not rise from pre-meal levels after a carbohydrate-rich meal with much more than 5% protein (Figure 2).

A delay of at least 2h after eating may be necessary for changes in neurotransmitter precursors to influence behavior. Earlier effects may be related to changes in glucose availability and levels of insulin and counter-regulatory hormones such as adrenaline, glucagon, and cortisol. These changes could underlie recent results after breakfasts of 20:80, 50:50, and 80:20 protein-carbohydrate ratios (1.67MJ, 400kcal). A measure of central attention initially improved after the carbohydrate-rich breakfast, but later improved after the protein-rich ones; the opposite was found for peripheral attention. This study also found that the 80% protein breakfast produced the best short-term memory performance about 1-2 h after eating, but not at 3.5 h.

Effects of dietary fat Most studies of the effects of fat have varied its level together with that of carbohydrate, while keeping protein constant and so allowing equicaloric meals. Comparisons have been made of low-fat (e.g., 11-29% of energy as fat), medium-fat (e.g., 45% of energy as fat), and high-fat (e.g., 56-74% of energy as fat) breakfasts, mid-morning and midday meals, and intraduodenal infusions of lipid or saline. On balance, high-fat meals appear to increase subsequent fatigue and reduce alertness and attention, relative to high-carbohydrate/low-fat meals. However, there are inconsistencies in changes in specific moods and the effects of meal timing: for instance, feelings of drowsiness, confusion, and uncertainty were found to increase after both low- and high-fat lunches but not after a medium-fat lunch. One possibility is that mood may be adversely affected by meals that differ substantially from habitual ones in macronutrient composition. An alternative is that similar mood effects could be induced (albeit by different mechanisms) by high carbohydrate in one meal and high fat in the other: for example, 1.67 MJ (400kcal) drinks of pure fat or carbohydrate taken in the morning both increased an objective measure of fatigue relative to a mixed-macronutrient drink, although the two single-nutrient drinks had opposite effects on plasma tryptophan/LNAA ratios.

In many of these studies, the meals were designed to disguise variation in fat level from the participants. It is therefore possible that effects on mood may have resulted from discrepancies between subjects' expectations of certain post-ingestive effects and the actual effects that resulted from neurohormonal responses to the detection of specific nutrients in the duodenum and liver. A case in point may be the increase in tension, 90 min after lunch, with increasing fat intake reported by predominately female subjects: this might reflect an aversive reaction to (unexpected) fat-related post-ingestive sensations.

Postprandial declines in arousal can be quite noticeable 2.5-3 h after high-fat meals, but fat in mid-morning meals seems to be more sedating than fat ingested at lunchtime, which might relate to expectations. By comparison, when lipid was infused directly into the duodenum, a decline in alertness was apparent much sooner, by 30-90 min after the meal. These effects of fat may result from increased release of the gastric regulatory hormone cholecystokinin. However, in a study comparing ingestion of pure fat, carbohydrate, and protein (1.67 MJ (400kcal) at breakfast), measures of memory, attention, and reaction time deteriorated more after carbohydrate and protein than after fat. This beneficial effect of fat was attributed to the demonstrated relative absence of glycemic and hormonal (insulin, glucagon, and cortisol) perturbations in the 3 h following fat ingestion.

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