Appetite Regulation And Stress-Related Eating
by Alan H. Pressman, D.C., D.A.C.B.N.
Note: The information on this website is¬† not a substitute¬† for the advice of¬† & treatment by a qualified professional.
The study of appetite regulation is primarily concerned with attempting to find a way to alter the inherent biological drive to eat. For several decades, researchers have been trying to pinpoint a primary mechanism within the body governing hunger and satiety in order to ascertain whether the selection of food has any specific physiological origin, or if there is even an overall caloric homeostasis in man. The outcome of work to date indicates that hunger is not the result of one single factor, but is instead elicited by many factors involved in a final common pathway.
In certain primitive societies, greater or lesser body mass was essential to survival. A long canoe trip across miles of ocean required that the traveler store food in his own body in the form of adipose tissue. In the African veldt, leanness was essential for the required quickness of running down and capturing prey on foot. In our modern, basically sedentary society, however, optimal weight is almost irrelevant for physical survival. It is instead involved with our concepts of health and longevity-and very often societal or cultural preferences. So-called normal weight, therefore, seems to be a concept dependent on the context to which it is applied.1
Today, fat people, although continuously preoccupied with food and eating, often do not know when they are hungry.2 For many, overeating and obesity serve the important function of avoiding emotions. Situations that provoke overeating and concomitant obesity resemble those that are usually accompanied by grief or severe depression.3 An individual who experiences every tension as a need to eat instead of feeling appropriate emotions such as anxiety or anger progressively gains weight. Disturbed hunger awareness is the main psychological deficit in some overweight individuals while others may have distorted feelings of sell-awareness. Attempts at weight reduction not only fail to solve their physical problems, but may induce additional feelings of frustration and stress. Many who attempt to reduce without inner emotional readiness eventually abandon the effort as too stressful. Others succeed without resolving their underlying psychological conflicts and become, as Hilde Bruch’s explains, “thin fat people,” the extreme of which is anorexia nervosa.4
The word anorexia is misleading since there is not true loss of appetite; the underlying disturbance is related more to not acknowledging hunger.5 In the advanced stages of emaciation, however, true loss of appetite may occur, similar to the disinterest in food during late stages of famine. Metabolically, the body goes into low gear, reverting to its pre-pubertal state, with many changes in metabolic and neuroendocrinal functioning.6 The effect on the psyche of severe undernutrition is largely responsible for the drawn-out course of the illness, sustaining it in many ways and making recognition and resolution of the underlying psychological issue difficult.7
Hunger and appetite are not solely behavioral phenomena since they have physiological bases as well. The integration of myriad impulses involved in appetite regulation takes place mainly in the complex structure sometimes called the brain’s brain, the hypothalamus. The signals transmitted to the hypothalamus include information about the circulating levels of various nutrients and feedback concerning the quantity of food present in the gastrointestinal tract. In addition, stimulation of the hypothalamus by a variety of physiological and psychological factors causes the autonomic nervous system to set off a chain of reactions that alter the functions of many glands and organs.
The hypothalamus performs its tasks through a complex pattern of many neurotransmitter substances including serotonin, the catecholamines (dopamine, norepinephrine, epinephrine), endogenous opiates and neuropeptides.8 The series of events which regulate food intake involves a delicate balance between these neural substances as well as the nutritional status of the organism. Research has shown that we obtain several precursor substrates from dietary sources, therefore many metabolic pathways are ultimately under nutritional control.9 Eating certain foods can raise the levels of these chemicals and actually increase the amplitude of the message sent, with behavioral consequences. In addition, diet-induced changes in plasma amino acids may directly alter the functional activity of brain neurons that mediate feeding behavior. Thus, the brain both controls and is controlled by an individual’s nutritional status.10
A well-known syndrome found in both animals and man is stress-induced eating. In the laboratory, stress-induced eating involved activation of the endogenous opioid systems.11,12 Various studies have shown that both exogenous and endogenous opiates can stimulate food intake.13,14 Opiate peptides have been shown to modulate responses to amino acid neurotransmitters. The implication is that dietary proteins, upon digestion, generate neuroactive peptides. In addition, alterations in carbohydrate metabolism have been shown to alter sensitivity of other receptors (e.g., dopoamine) thought to be involved in feeding. Dome neuropeptides released prior to or after a meal regulate temperature. This phenomenon explains the interrelationship between external temperature regulation and food intake (the thermostatic hypothesis)15 and why a person with a fever has little desire to eat.
It has been reported that obese mice and rats have an increased level of B-endorphin within the pituitary as well as being more sensitive to naloxone-induced suppression of feeding. (Naloxone is a specific opiate antagonist.) Opiates, moreover, appear preferentially to stimulate the intake of foods with a high energy content.16 After ten days with several episodes of stress-induced eating per day, there is a withdrawal syndrome similar to that seen after opiate addication, which supports the concept that obesity may result from autoaddiction to endogenous opioid peptides.11
Changes in circulating glucose levels modulate the response to opiate antagonism of feeding, which relates to Mayer’s well-known glucostatic theory.17 Glucose interacts directly with the opiate receptor, altering its ability to bind the endogenous opiates. Animals with high blood sugar levels are extremely sensitive to naxolone-induced suppression of food intake. On the other hand, feeding brought about by insulin-induced hypoglycemia is resistant to the suppressive effect of naxolone.18,19
Another important factor in the understanding of appetite regulation in stress-induced eating is the isolation of the neuropeptide. corticotrophinreleasing factor (CRF). CRF releases adrenocorticotrophic hormone and B-endorphin and increases heart rate, mean arterial blood pressure and is therefore involved in stress-related phenomena. CRF seems to fulfill Han Selye’s criteria for the central mediator of his general adaptation-to-stress syndrome. As we have seen, stress can result in either increased feeding or anorexia. Anorectics are know to have overactive hypothalamic-pituitaryadrenal functions, which might mean that the defect is an increase in CRF. Depressed patients, many of whom are arnorectic, also have a non-supressible pituitary-adrenal axis, suggesting the possibility of increased CRF function.20 Thus, it seems stress can produce either overeating through activation of the endogenous opioid system or decreased eating through a rise in CRF activity.
Several different types of abnormal eating patterns have been observed in stressed individuals.21 One is the night-eating syndrome, characterized by evening hyperphagia and morning anorexia. It occurs during periods of life stress and disappears with relief of that stress, and is sometimes related to the development of obesity. Interestingly, studies on the circadian variation in endogenous opiate levels due to fluctuations in normal rhythmic biologic cycles in rats have shown that the highest levels occur during the nocturnal feeding phase with lowest levels during the daytime phase of the cycle.22
Another abnormal eating pattern is binge eating, which also occurs during periods of life stress. It is characterized by the ingestion of large amounts of food in a short period of time, typically followed by feelings of self-condemnation and guilt and self-induced vomiting. Binge eating occurs more in people who keep their weight at an abnormally low level than in overweight people; many binge eaters are anorectic. Such periods of active overeating are associated with extreme degrees of inactivity.21
Obesity and anorexia are the two pathological and opposite poles of stress-related eating. More common eating variations are conscious attempts to lose weight by fasting and overeating in certain cultural milieus. Occasionally, fasting and overeating go hand in hand, as observed in the night-eating and binge eating syndromes.
Some recent studies have focused on the role of the sympathetic nervous system in the metabolic adaptation to fasting and overfeeding. Contrary to expectations, researchers found that fasting suppresses sympathetic activity and conserves calories by diminishing metabolism and heat production, resulting in a resistance to weight loss during therapeutic fasting.23,24
Conservation of fuel and energy during fasting is an important biological survival mechanism; therefore stimulation of metabolic processes by catecholamines would be detrimental to overall metabolic homeostasis when available calories are limited. Catecholamines mobilize fuels in situations associated with an increase in total energy use, but are not responsible for fuel mobilization in the fasting state when total energy use is reduced.25
Some researchers have cautioned that it is potentially dangerous to enforce weight reduction in people with circulatory disorders. If overweight individuals maintain the weight they have lost, the ensuing restoration of weight places a damaging burden on circulation.26 Changes in sympathetic activity may partly explain the relationship between cardiovascular disease and nutrition. Increased sympathetic activity may account for some of the increased incidence of arrhythmias, angina and hypertension in populations in which overeating is common. Arrhythmias are fatal in some patients during post-fast refeeding.27 In patients with underlying heart disease, arrhythmias could result from an abrupt increase in sympathetic activity to the heart. Conversely, hypotension and poor resistance to a variety of pathophysiological stresses that occur in chronic starvation may result from suppression of the sympathetic nervous system.28
Stress is an unavoidable fact of life in contemporary society. Stress related problems are exacerbated in people whose diets fail to provide the extra nutrients their bodies need to deal with the heavy demands of stressful situations. Just the normal biochemical needs of uncomplicated daily living can often provoke severe symptoms when nutritional deficiencies have compounded over the years. And abnormal neural or glandular functions can result from long-standing deficiencies.
Stress nutrition is a program specifically designed to combat stress dysfunction and attempts to meet individual biochemical requirements by providing the right amount of each nutrient in proportion to every other nutrient. It is important to determine not only what vitamins and minerals a person is deficient in and to what degree, but also if there are any problems on the neuroendocrinal level. Not only is it essential to curtail intake of sugar, fats, carbohydrates, processed foods, refined foods, alcohol, cigarettes and pharmaceuticals, but equally important is consuming a diet balanced to the individual’s particular nutrient requirements. People under stress are often deficient in the B vitamins, particularly pyrodoxine and pantothenic acid, as well as vitamin C and the minerals calcium, magnesium and zinc. Stress nutrition not only deals with diet in its program, but might include exercise, behavior modification or biofeedback.
In a complex biochemical system such as man, many factors are involved in the acquisition and consumption of food. Diverse signals can originate in the brain, in the periphery, or they can develop as a habit. In addition, factors such as emotions, perceptual differences and eating disorders can play a role in modifying the signals used to initiate feeding. Though each separate factor can be manipulated to initiate eating, there appears to be no one single primary mechanism that can be called the “hunger” mechanism.
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