Effect of Food Composition and Intake on the Ability to Cope with Stress

Research on the biological and psychological effects of varying food intake has focused on two main areas. First, there has been interest in the behavioral effects of dieting. Second, there has been interest in the effects of dieting on biological parameters, some of which may affect the ability to cope with stress.

Research in the latter area has focused on the effects of dieting on the neurotransmitter 5-HT. 5-HT is biologically unusual in that the rate of its synthesis is entirely dependent on the supply of its essential amino acid precursor, tryptophan, in food. Furthermore, the availability of tryptophan to the brain depends on the balance of macronutrients (carbohydrate, protein, and fat).

Dieting is a very common behavior in Western cultures. Approximately 25% of men and 40% of women in the United Sates report that they are currently trying to lose weight. Dieting seems to be particularly common among adolescent girls, but the rates are higher at all ages in women compared with men.

Behavioral Effects of Dieting. The first direct evidence on the behavioral effects of food restriction came from a study of World War II conscientious objectors who were placed on a 24-week semistarvation diet. The main findings were an increase in lethargy, tiredness, depression, and irritability and a lowering of energy. In contrast, other studies using less extreme dietary restriction have found less dramatic changes in mood.

Several studies have shown that dieters perform less well on cognitive tasks. Dieting impairs sustained attention and short-term recall and results in slower reaction times. Nondieters with high levels of restraint over eating showed intermediate cognitive performance between dieters and low restraint nondieters. Impairments in cognitive functioning, such as impaired vigilance, have also been noted among subjects with bulimia nervosa and anorexia nervosa, probably due to restricted eating.

Dieting itself affects eating behavior. In a series of well-replicated studies, Polivy and Herman showed that dieters failed to compensate for a modest calorie loading by decreasing their caloric intake at the next meal.

They actually ate more after the preload than after no preload; they counterregulated rather than showing the normal compensatory regulation seen in the controls. It has been widely argued that counterregulation is a result of the preload causing disinhibition and abandoning of dietary restraint in the dieter. This cognitive explanation is supported by the finding that dieters also counterregulate when they perceive the preload as high in calories, regardless of the actual calorie content.

Severe dietary restriction in normal controls can result in binge eating. The World War II study of conscientious objectors described earlier also investigated the effects of refeeding. The men returned to their normal weights after the study but exhibited a persistent tendency to binge eat. This type of behavior had not occurred prior to the study.

Healthy volunteer studies during short-term calorie-controlled diets show that subjects have increased preoccupation with thoughts of food, urges to eat more frequently, and feelings of being out of control with their eating. Rates of postwar binge eating in World War II combat veterans and prisoners of war show that binge eating is significantly more prevalent in veterans who lost large amounts of weight during their captivity.

Thus, dietary restriction and normal dieting have significant effects on behaviors such as food intake, mood, and cognitive functioning. There has been debate, however, about how these effects are mediated. One possibility is that dieting alters 5-HT function, discussed next.

Dieting and 5-HT. The rate of synthesis of 5-HT in the brain is critically dependent on the amount of its precursor, tryptophan, which is able to enter the brain. Tryptophan is available solely from the diet, and its availability in the brain can be critically affected by alterations in food intake, particularly in the balance of macronutrients.

Tryptophan competes for entry to the brain across the blood-brain barrier with other amino acids (components of protein). Any change in food intake that alters this ratio of tryptophan to other amino acids will directly affect the amount of 5-HT synthesized.

Studies of the effects of a standard 3 week, 1000 kcal diet have shown that the diet results in a lowering of tryptophan in the plasma (blood). The key question is whether this affects 5-HT function itself. Studies using a variety of challenge tests for different aspects of 5-HT function show that it does, although the effect is significant only in women.

It seems that female dieters can compensate to some extent for the reduction in 5-HT synthesis induced by dieting, but it is likely that dieting results in a reduction in 5-HT function. Because this effect is gender specific, women may be biologically more vulnerable to the effects of dieting on 5-HT function.

What might be the consequences of this lowered 5-HT function after dieting? First, decreased 5-HT function will reduce satiety and increase the drive to eat. This may be one of the reasons why it is often reported that dieting is difficult to sustain. Some subjects who are dieting report craving carbohydrate or even bingeing on high-carbohydrate, low-protein foods.

Wurtman and colleagues have proposed that this craving may be explained by the fact that these foods increase 5-HT function indirectly. This occurs because a carbohydrate-rich meal causes secretion of the hormone insulin, increasing the ratio of tryptophan to other amino acids and an increase in the entry of tryptophan to the brain. The end result is an increase in the synthesis of 5-HT, which to some extent may correct the deficit induced by dieting.

It is also possible that the reduction in 5-HT function might affect mood. Experimental work using an artificial mixture of amino acids to temporarily lower 5-HT synthesis has shown that this can induce symptoms of depression, but only in women who have a strong previous history of depression. Animal and human work suggests that a key role of 5-HT is to promote resilience in the face of stressful circumstances.

Failure of this system, thus reducing a person’s ability to deal effectively with a stressful life event, may be one of the key factors contributing to the onset of depression. If dieting impairs 5-HT function directly, it may contribute to the onset of depression after a stressful life event.

However, this may occur only in those people who have a vulnerability to depression because of their heredity or past history. Further research on the effects of dieting, particularly in people at risk of depression or eating problems, will need to performed before this hypothesis can be confirmed.

Food Shift Effect

Endogenous Circadian Clocks. In 1972, the neural substrate responsible for the generation and entrainment of circadian rhythms by light was identified. Lesions of this small structure, the suprachiasmatic nucleus (SCN) of the hypothalamus, appeared to abolish circadian rhythms in behavior and physiology.

However, despite such lesions, rats were still able to anticipate one meal per day by increased activity, a rise in core temperature and serum corticosterone, and other physiological changes that occurred approximately 2-4 h prior to meal access.

There is now compelling evidence that these functions are mediated by an endogenous circadian clock: (1) meal anticipation occurs only if the interval between meals is in the circadian range (-22-30 h), (2) anticipatory activity persists for several days when rats are food-deprived or the activity free runs (in some rats) if meals are presented outside the circadian range, and (3) phase shifts of meal-time result in transients, that is, gradual daily adjustments until the activity reentrains to the new meal time (see Figure 1).

Figure 1. Anticipatory wheel running from a rat with a lesion of the suprachiasmatic nucleus (arrhythmic when fed ad libitum). Food is available for 2 h day^-1, indicated by the vertical crosshatched bars. Most wheel running occurs approximately 3 h before meal time. When the meal time is delayed by 8 or 10 h, anticipatory activity takes 3 or 4 days to reentrain to the phase-shifted meal. The activity persists during food deprivation (FD), but is not observed during ad libitum (AL) feeding

Despite many efforts, this feeding-entrained oscillator (FEO) has not yet been localized. Nevertheless, most mammals, as well as some inframammalian species, are now known to have the capacity to anticipate daily meals, and it would be surprising if humans lacked such a circadian clock.

It is well known that hunger sensations arise around the customary meal time. What has been difficult to explain from a purely homeostatic view is that the omission of a meal does not produce monotonically increasing feelings of hunger; instead, hunger subsides until the next customary meal time. However, this makes sense if hunger sensations are based in part on an internal timing signal and not entirely on an energy-deficit signal.

Physiological Correlates of Entrainment by Meals. Before addressing the potentially adverse effects of changes in meal time or meal omission, a brief summary of the main effects of feeding one meal per day on the rat’s digestive physiology is in order. As mentioned earlier, serum corticosterone levels rise prior to expected meals.

Corticosterone is both a metabolic and a stress hormone, and the brain has receptors for this steroid. Perhaps most surprising is the observation that disaccharidases (enzymes for digesting sugars) in the duodenum also increase before the meal is available. In addition, several aspects of liver function, cell division in the gastrointestinal tract, and intestinal motility become entrained to periodic meals. The increase in core temperature also may facilitate digestion.

The general inference to be drawn from these observations is that the digestive physiology is not simply reactive to ingested nutrients but is capable of anticipating and preparing for meals, most likely under the influence of the circadian FEO. If the expected meal is displaced in time, these efforts are for naught and for several days these preparatory responses are out of synchrony with actual food consumption.