Eating is essential for survival, and it is no surprise that a drive like hunger exists to ensure that we seek out sustenance. While this chapter will focus primarily on the physiological mechanisms that regulate hunger and eating, powerful social, cultural, and economic influences also play important roles. This section will explain the regulation of hunger, eating, and body weight, and we will discuss the adverse consequences of disordered eating.
Physiological Mechanisms of Hunger and Eating
There are a number of physiological mechanisms that serve as the basis for hunger. When our stomachs are empty, they contract. Typically, a person then experiences hunger pangs. Chemical messages travel to the brain, and serve as a signal to initiate feeding behaviour. When our blood glucose levels drop, the pancreas and liver generate a number of chemical signals that induce hunger (Konturek et al., 2003; Novin, Robinson, Culbreth, & Tordoff, 1985) and thus initiate feeding behaviour.
For most people, once they have eaten, they feel satiation, or fullness and satisfaction, and their eating behaviour stops. Like the initiation of eating, satiation is also regulated by several physiological mechanisms. As blood glucose levels increase, the pancreas and liver send signals to shut off hunger and eating (Drazen & Woods, 2003; Druce, Small, & Bloom, 2004; Greary, 1990). The food’s passage through the gastrointestinal tract also provides important satiety signals to the brain (Woods, 2004), and fat cells release leptin, a satiety hormone.
The various hunger and satiety signals that are involved in the regulation of eating are integrated in the brain. Research suggests that several areas of the hypothalamus and hindbrain are especially important sites where this integration occurs (Ahima & Antwi, 2008; Woods & D’Alessio, 2008). Ultimately, activity in the brain determines whether or not we engage in feeding behaviour (Figure EM.9).
The hypothalamus (located in the lower, central part of the brain) plays a very important role in eating behaviour. It is responsible for synthesizing and secreting various hormones. The lateral hypothalamus (LH) is concerned largely with hunger and, in fact, lesions (i.e., damage) of the LH can eliminate the desire for eating entirely—to the point that animals starve themselves to death unless kept alive by force feeding (Anand & Brobeck, 1951). Additionally, artificially stimulating the LH, using electrical currents, can generate eating behaviour if food is available (Andersson, 1951).
Hunger is only part of the story of when and why we eat. A related process, satiation, refers to the decline of hunger and the eventual termination of eating behaviour. Whereas the feeling of hunger gets you to start eating, the feeling of satiation gets you to stop. Perhaps surprisingly, hunger and satiation are two distinct processes, controlled by different circuits in the brain and triggered by different cues. Distinct from the LH, which plays an important role in hunger, the ventromedial hypothalamus (VMH) plays an important role in satiety (more on this in the tricky topic below). Though lesions of the VMH can cause an animal to overeat to the point of obesity, the relationship between the LH and the VMB is quite complicated.
The physical sensation of hunger comes from contractions of the stomach muscles. These contractions are believed to be triggered by high concentrations of the hormone ghrelin. Two other hormones, peptide YY and leptin, cause the physical sensations of being full. Ghrelin is released if blood sugar levels get low, a condition that can result from going long periods without eating.
Long-Term Hunger Regulation
The long-term regulation of hunger prevents energy shortfalls and is concerned with the regulation of body fat. Leptin, a hormone secreted exclusively by adipose cells in response to an increase in body-fat mass, helps regulate long-term hunger and food intake. Leptin serves as the brain’s indicator of the body’s total energy stores. The function of leptin is to suppress the release of neuropeptide Y (NPY), which in turn prevents the release of appetite-enhancing orexins from the lateral hypothalamus. This decreases appetite and food intake, promoting weight loss. Though rising blood levels of leptin do promote weight loss to some extent, its main role is to protect the body against weight loss in times of nutritional deprivation.
Short-Term Hunger Regulation
The short-term regulation of hunger deals with appetite and satiety. It involves neural signals from the GI tract, blood levels of nutrients, and GI-tract hormones.
Neural Signals from the GI Tract
The brain can evaluate the contents of the gut through vagal nerve fibres that carry signals between the brain and the gastrointestinal (GI) tract. Studies have shown that the brain can sense differences between macronutrients through these vagal nerve fibres. Stretch receptors (mechanoreceptors that respond to an organ being stretched or distended) work to inhibit appetite when the GI tract becomes distended. They send signals along the vagus nerve afferent pathway and ultimately inhibit the hunger centres of the hypothalamus.
Blood levels of glucose, amino acids, and fatty acids provide a constant flow of information to the brain that may be linked to regulating hunger and energy intake. Nutrient signals indicate fullness. They inhibit hunger by raising blood glucose levels, elevating blood levels of amino acids, and affecting blood concentrations of fatty acids.
Hormones can have a wide range of effects on hunger. The hormones insulin and cholecystokinin (CCK) are released from the GI tract during food absorption and act to suppress feelings of hunger. However, during fasting, glucagon and epinephrin levels rise and stimulate hunger. When blood sugar levels fall, the hypothalamus is stimulated. Ghrelin, a hormone produced by the stomach, triggers the release of orexin from the hypothalamus, signalling to the body that it is hungry.
Metabolism and Body Weight
Our body weight is affected by a number of factors, including gene-environment interactions, and the number of calories we consume versus the number of calories we burn in daily activity. If our caloric intake exceeds our caloric use, our bodies store excess energy in the form of fat. If we consume fewer calories than we burn off, then stored fat will be converted to energy. Our energy expenditure is obviously affected by our levels of activity, but our body’s metabolic rate also comes into play. A person’s metabolic rate is the amount of energy that is expended in a given period of time, and there is tremendous individual variability in our metabolic rates. People with high rates of metabolism are able to burn off calories more easily than those with lower rates of metabolism.
We all experience fluctuations in our weight from time to time, but generally, most people’s weights fluctuate within a narrow margin, in the absence of extreme changes in diet and/or physical activity. This observation led some to propose a set-point theory of body weight regulation. The set-point theory asserts that each individual has an ideal body weight, or set point, which is resistant to change. This set-point is genetically predetermined and efforts to move our weight significantly from the set-point are resisted by compensatory changes in energy intake and/or expenditure (Speakman et al., 2011).
Some of the predictions generated from this particular theory have not received empirical support. For example, there are no changes in metabolic rate between individuals who had recently lost significant amounts of weight and a control group (Weinsier et al., 2000). In addition, the set-point theory fails to account for the influence of social and environmental factors in the regulation of body weight (Martin-Gronert & Ozanne, 2013; Speakman et al., 2011). Despite these limitations, set-point theory is still often used as a simple, intuitive explanation of how body weight is regulated. See Psychological Disorders for further discussion about eating disorders.
Being extremely overweight or obese is a risk factor for several negative health consequences. These include, but are not limited to, an increased risk for cardiovascular disease, stroke, Type 2 diabetes, liver disease, sleep apnea, colon cancer, breast cancer, infertility, and arthritis. Given that it is estimated that in the United States around one-third of the adult population is obese and that nearly two-thirds of adults and one in six children qualify as overweight (CDC, 2012), there is substantial interest in trying to understand how to combat this important public health concern.
Prader-Willi Syndrome (PWS) is a genetic disorder that results in persistent feelings of intense hunger and reduced rates of metabolism. Typically, affected children have to be supervised around the clock to ensure that they do not engage in excessive eating. Currently, PWS is the leading genetic cause of morbid obesity in children, and it is associated with a number of cognitive deficits and emotional problems (Figure EM.12).
While genetic testing can be used to make a diagnosis, there are a number of behavioural diagnostic criteria associated with PWS. From birth to 2 years of age, lack of muscle tone and poor sucking behaviour may serve as early signs of PWS. Developmental delays are seen between the ages of 6 and 12, and excessive eating and cognitive deficits associated with PWS usually onset a little later.
While the exact mechanisms of PWS are not fully understood, there is evidence that affected individuals have hypothalamic abnormalities. This is not surprising, given the hypothalamus’s role in regulating hunger and eating. However, as you will learn in the next section of this chapter, the hypothalamus is also involved in the regulation of sexual behaviour. Consequently, many individuals suffering from PWS fail to reach sexual maturity during adolescence.
There is no current treatment or cure for PWS. However, if weight can be controlled in these individuals, then their life expectancies are significantly increased (historically, sufferers of PWS often died in adolescence or early adulthood). Advances in the use of various psychoactive medications and growth hormones continue to enhance the quality of life for individuals with PWS (Cassidy & Driscoll, 2009; Prader-Willi Syndrome Association, 2012).
While nearly two out of three US adults struggle with issues related to being overweight, a smaller, but significant, portion of the population has eating disorders that typically result in being normal weight or underweight. Often, these individuals are fearful of gaining weight. Individuals who suffer from bulimia nervosa and anorexia nervosa face many adverse health consequences (Mayo Clinic, 2012a, 2012b).
People suffering from bulimia nervosa engage in binge eating behaviour that is followed by an attempt to compensate for the large amount of food consumed. Purging the food by inducing vomiting or through the use of laxatives are two common compensatory behaviours. Some affected individuals engage in excessive amounts of exercise to compensate for their binges. Bulimia is associated with many adverse health consequences that can include kidney failure, heart failure, and tooth decay. In addition, these individuals often suffer from anxiety and depression, and they are at an increased risk for substance abuse (Mayo Clinic, 2012b). The lifetime prevalence rate for bulimia nervosa is estimated at around 1% for women and less than 0.5% for men (Smink, van Hoeken, & Hoek, 2012).
As of the 2013 release of the Diagnostic and Statistical Manual, fifth edition, Binge eating disorder is a disorder recognized by the American Psychiatric Association (APA). Unlike with bulimia, eating binges are not followed by inappropriate behaviour, such as purging, but they are followed by distress, including feelings of guilt and embarrassment. The resulting psychological distress distinguishes binge eating disorder from overeating (American Psychiatric Association [APA], 2013).
Anorexia nervosa is an eating disorder characterized by the maintenance of a body weight well below average through starvation and/or excessive exercise. Individuals suffering from anorexia nervosa often have a distorted body image, referenced in literature as a type of body dysmorphia, meaning that they view themselves as overweight even though they are not. Like bulimia nervosa, anorexia nervosa is associated with a number of significant negative health outcomes: bone loss, heart failure, kidney failure, amenorrhea (cessation of the menstrual period), reduced function of the gonads, and in extreme cases, death. Furthermore, there is an increased risk for a number of psychological problems, which include anxiety disorders, mood disorders, and substance abuse (Mayo Clinic, 2012a). Estimates of the prevalence of anorexia nervosa vary from study to study but generally range from just under one percent to just over four percent in women. Generally, prevalence rates are considerably lower for men (Smink et al., 2012).
While both anorexia and bulimia nervosa occur in people of many different cultures, Caucasian females from Western societies tend to be the most at-risk population. Recent research indicates that females between the ages of 15 and 19 are most at risk, and it has long been suspected that these eating disorders are culturally-bound phenomena that are related to messages of a thin ideal often portrayed in popular media and the fashion world (Figure EM.13) (Smink et al., 2012). While social factors play an important role in the development of eating disorders, there is also evidence that genetic factors may predispose people to these disorders (Collier & Treasure, 2004).