Understanding Hunger

There are a number of physiological mechanisms that serve as the basis for hunger. When our stomachs are empty, they contract, causing both hunger pangs and the secretion of chemical messages that travel to the brain to 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 1).

Figure 1. 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; 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).

Obesity

One common measure of health and body weight, and to differentiate the status of someone’s weight from underweight, normal, overweight, and obese is the Body Mass Index (BMI).

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 2). An adult with a Body Mass Index (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 morbidly obese. Morbid obesity is defined as having a BMI over 40.

However, it should be noted that recently the utility of the BMI has been questioned.^[1] Specifically, the 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.

Figure 2. 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.

Being extremely overweight or obese is a risk factor for several negative health consequences. Negative health consequences 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 around one-third of the adult U.S. 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.

Dig Deeper: Prader-Willi Syndrome

Figure 3. Eugenia Martínez Vallejo, depicted in this 1680 painting, may have had Prader-Willi syndrome. At just eight years old, she weighed approximately 120 pounds, and she was nicknamed “La Monstrua” (the monster).

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.

While genetic testing can be used to make a diagnosis, there is a number of behavioral diagnostic criteria associated with PWS. From birth to two 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 six 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 module, 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).