Skip to ContentGo to accessibility pageKeyboard shortcuts menu
OpenStax Logo
Psychology 2e

10.2 Hunger and Eating

Psychology 2e10.2 Hunger and Eating

Learning Objectives

By the end of this section, you will be able to:

  • Describe how hunger and eating are regulated
  • Differentiate between levels of overweight and obesity and the associated health consequences
  • Explain the health consequences resulting from anorexia and bulimia nervosa

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

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 behavior. 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 behavior.

For most people, once they have eaten, they feel satiation, or fullness and satisfaction, and their eating behavior 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 behavior (Figure 10.9).

An outline of the top half of a human body contains illustrations of the brain and the stomach in their relative locations. A line extends from the location of the hypothalamus in the brain illustration, out to the left, past the outline, where it meets a box labeled “Hunger.” Down-facing arrows connect that box to a box labeled “Food,” and the box labeled “Food” to a box labeled “Satiety.” A line extends out to the right from the box labeled “Satiety,” and meets with the illustration of the stomach.
Figure 10.9 Hunger and eating are regulated by a complex interplay of hunger and satiety signals that are integrated in the brain.

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.

Obesity

When someone weighs more than what is generally accepted as healthy for a given height, they are considered overweight or obese. According to the Centers for Disease Control and Prevention (CDC), an adult with a body mass index (BMI) between 25 and 29.9 is considered overweight (Figure 10.10). An adult with a BMI of 30 or higher is considered obese (Centers for Disease Control and Prevention [CDC], 2012). People who are so overweight that they are at risk for death are classified as severely obese. Severe obesity is defined as having a BMI over 40. Note that although BMI has been used as a healthy weight indicator by the World Health Organization (WHO), the CDC, and other groups, its value as an assessment tool has been questioned. The BMI is most useful for studying populations, which is the work of these organizations. It is less useful in assessing an individual since height and weight measurements fail to account for important factors like fitness level. An athlete, for example, may have a high BMI because the tool doesn’t distinguish between the body’s percentage of fat and muscle in a person’s weight. BMI scales have not accounted for differences in body composition related to race or ethnicity; as a result, BMI is less useful in determining health of all people. While many healthcare professionals and organizations still utilize BMI, the American Medical Association in 2023 recommended that it be removed as a standard measure of health.

A chart has an x-axis labeled “weight” (pounds/kilograms) and a y-axis labeled “height” (meters and feet/inches). Four areas are shaded different colors indicating the BMI for ranges of weight and height. The “underweight BMI <18.5” area begins at approximately 90 pounds and 4’11” and extends to approximately 160 pounds and 6’6”. The “normal range BMI 18.5–25” area covers approximately 90–120 pounds at height 4’11” and extends to approximately 160–220 pounds at height 6’6”. The “overweight BMI 25–30” area covers approximately 120–140 pounds at height 4’11” and extends to approximately 220–265 pounds at height 6’6”. The “obese range BMI >30” area covers approximately 140–350 pounds at height 4’11” and extends to approximately 265–350 pounds at height 6’6.”
Figure 10.10 This chart shows how adult BMI is calculated. Individuals find their height on the y-axis and their weight on the x-axis to determine their BMI. While BMI is widely used and does provide some indications of health, it does not account for differences in people's body composition. The American Medical Association has recommended it be de-emphasized as a measure of health.

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 forty percent of the adult population is obese and that nearly three-quarters of adults and one in six children qualify as overweight (CDC, 2018), there is substantial interest in trying to understand how to combat this important public health concern.

What causes someone to be overweight or obese? You have already read that both genes and environment are important factors for determining body weight, and if more calories are consumed than expended, excess energy is stored as fat. However, socioeconomic status and the physical environment must also be considered as contributing factors (CDC, 2012). For example, an individual who lives in a neighborhood with high crime rates and few food options may never feel comfortable walking or biking to work or to the local market. This might limit the amount of physical activity in which they engage. Similarly, some people may not be able to afford healthy food options from their market, or these options may be unavailable (especially in urban areas or poorer neighborhoods); therefore, some people must rely primarily on available, inexpensive, high fat, and high calorie fast food as their primary source of nutrition.

Generally, people are encouraged to try to maintain and improve health through a combination of both diet and exercise. While some people are very successful with these approaches, many are not. In cases in which a person has had no success with repeated attempts to reduce weight or is at risk for death because of obesity, bariatric surgery may be recommended. Bariatric surgery is a type of surgery specifically aimed at weight reduction, and it involves modifying the gastrointestinal system to reduce the amount of food that can be eaten and/or limiting how much of the digested food can be absorbed (Figure 10.11) (Mayo Clinic, 2013). A recent meta-analysis suggests that bariatric surgery is more effective than non-surgical treatment for obesity in the two-years immediately following the procedure, but to date, no long-term studies yet exist (Gloy et al., 2013).

An illustration depicts a gastric band wrapped around the top portion of a stomach. A bulging area directly above the gastric band is labeled “Small stomach pouch.” The area directly below the stomach is labeled “Duodenum.” Down-facing arrows indicate the direction in which digested food travels from the esophagus at the top, down through the stomach, and into the duodenum.
Figure 10.11 Gastric banding surgery creates a small pouch of stomach, reducing the size of the stomach that can be used for digestion.

Dig Deeper

Prader-Willi Syndrome

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 severe obesity in children, and it is associated with a number of cognitive deficits and emotional problems (Figure 10.12).

A painting shows Eugenia Martínez Vallejo.
Figure 10.12 Eugenia Martínez Vallejo, depicted in this 1680 painting, may have had Prader-Willi syndrome. At just eight years old, she weighed approximately 120 pounds.

While genetic testing can be used to make a diagnosis, there are a number of behavioral diagnostic criteria associated with PWS. From birth to 2 years of age, lack of muscle tone and poor sucking behavior 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 behavior. 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).

Eating Disorders

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 underweight. Often, these individuals are fearful of gaining weight. Individuals who have bulimia nervosa and anorexia nervosa face many adverse health consequences (Mayo Clinic, 2012a, 2012b).

People suffering from bulimia nervosa engage in binge eating behavior 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 behaviors. 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 behavior, 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 with 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 from many different cultures, White 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 10.13) (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).

A photograph shows a very thin model.
Figure 10.13 Young people in our society are inundated with images of extremely thin models (sometimes accurately depicted and sometimes digitally altered to make them look even thinner). These images may contribute to eating disorders. (credit: Peter Duhon)
Order a print copy

As an Amazon Associate we earn from qualifying purchases.

Citation/Attribution

This book may not be used in the training of large language models or otherwise be ingested into large language models or generative AI offerings without OpenStax's permission.

Want to cite, share, or modify this book? This book uses the Creative Commons Attribution License and you must attribute OpenStax.

Attribution information
  • If you are redistributing all or part of this book in a print format, then you must include on every physical page the following attribution:
    Access for free at https://openstax.org/books/psychology-2e/pages/1-introduction
  • If you are redistributing all or part of this book in a digital format, then you must include on every digital page view the following attribution:
    Access for free at https://openstax.org/books/psychology-2e/pages/1-introduction
Citation information

© Jan 6, 2024 OpenStax. Textbook content produced by OpenStax is licensed under a Creative Commons Attribution License . The OpenStax name, OpenStax logo, OpenStax book covers, OpenStax CNX name, and OpenStax CNX logo are not subject to the Creative Commons license and may not be reproduced without the prior and express written consent of Rice University.