Chapter 8: Regulation of Energy Intake

Learning Objectives

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

  • Describe factors that contribute to hunger and satiety.
  • Name a hormone that increases hunger and three that increase satiety.

Physiology

The deceptively simple behavior of eating has both biological and social determinants. Biologically, hunger is controlled by the complex pathways of the nervous system and the hormonal systems in the brain and body. The thought, “my stomach is growling,” is the result of a more complicated process than it seems!

Influences on eating: biological, psychological, social-cultural. Read text for more details.
Figure 8.1: Biological, Psychological, and Social-Cultural Contributors to Eating. Credit: Introduction to Psychology – 1st Canadian Edition. CC BY-NC-SA 4.0

The hypothalamus in the brain is the main control point of hunger and satiety. It receives hormonal and neural signals, which determine if you feel hungry or full. Hunger is an unpleasant sensation caused by the body’s need for food; is communicated to the brain by mechanical and chemical signals from peripheral organs. Conversely, satiety is the sensation of feeling “full” or not needing food; it also is influenced by mechanical and chemical signals from the periphery. Two areas of the hypothalamus are known to be particularly important in eating. The lateral part of the hypothalamus responds primarily to cues to start eating, whereas the ventromedial part of the hypothalamus primarily responds to cues to stop eating. If the lateral part of the hypothalamus is damaged, the animal will not eat even if food is present, whereas if the ventromedial part of the hypothalamus is damaged, the animal will eat until it is obese[1].

Interestingly, communication between the gastrointestinal (GI) tract (also called the ‘gut’ for short) and the brain goes both ways. The brain can send signals to the digestive system via the vagus nerve, also called cranial nerve X. This nerve also carries information about fullness and nutrient composition from the digestive system to the brain.

The gut also communicates with the hypothalamus using hormones. Some of these hormones are shown in Table 8.1. Ghrelin is secreted by the stomach when it is empty; it stimulates hunger and makes animals (including humans) seek food. Hormones that inhibit hunger and promote satiety include cholecystokinin (CCK) released from the upper small intestine when it detects fat and protein, insulin released from the pancreas when it detects sufficient blood glucose, and peptide YY (PYY) released by the colon in response to the presence of fat and protein. Other hormones that affect hunger and satiety include amylin, glucagon-like polypeptide 1, pancreatic polypeptide, and oxyntomodulin.

Table 8.1 Hormonal regulators of hunger and satiety

Hormone

Secreted from

Stimulus for secretion

Effect

Ghrelin

stomach

empty stomach

increases hunger

Cholesystokinin

upper small intestine

fat or protein entering small intestine

decreases hunger

Insulin

pancreas

rise in blood glucose

decreases hunger

Peptide YY

colon

presence of fat and protein in food

decreases hunger

Leptin

adipose tissue

increased amounts of fat stored in body

increases satiety

Adipose (fat) tissue also plays a role in regulating food intake. Adipose tissue produces the hormone leptin in response to the increase in fat stores. Leptin stimulates the satiety region of the hypothalamus, which lowers the desire for food. Mice that are unable to make leptin show excessive food consumption and become obese (Figure 8.2).

Leptin-deficient mice (left) exhibit excessive food consumption and diet-induced obesity compared to normal mice (right).
Figure 8.2 Leptin-deficient mice (left) exhibit excessive food consumption and diet-induced obesity compared to normal mice (right). Source: Fatmouse by Sunholm, via Wikimedia Commons, public domain.

The discovery of leptin’s functions led to excitement as it was hypothesized that doses of leptin might decrease food intake. Unfortunately, it doesn’t seem to be that simple. Several clinical trials indicate that people who are overweight or obese are resistant to the hormone, meaning their brain does not respond as well to it[2]. Administering leptin to an overweight or obese person does not have a sustained effect on food intake.

Nutrients from food, as they circulate in the bloodstream, also influence food intake. The hypothalamus senses nutrient levels in the blood. Low nutrient levels stimulate the hunger center, and high levels stimulate the satiety center. Researchers are investigating links between hormone levels and cravings for salty and sweet foods. Both undernutrition and overnutrition affect hormone levels and the neural circuitry controlling hunger, which makes losing or gaining weight a substantial physiological hurdle.

Genetic Influences

Genes appear to have a role in body mass and composition as well as food intake. Although the environment where a child lives is important, adopted children resemble their biological parents in many physical characteristics. More evidence for the power of genetics is seen in twin studies; identical twins are more likely to be of similar weights than fraternal twins. The search for obesity genes has identified a few, such as the genes for leptin and the leptin receptor. Individuals with defects in these genes are rare, however, while obesity is common worldwide.

The current hypothesis about genes and obesity is that many genes are involved, and the interaction with the environment is complex. As much as 70% of the risk of obesity may be genetic[3]. Modern humans evolved in an environment in which food might be scarce or inconsistent; a feast after a successful hunt or fruit harvest might be followed by weeks of poor food supply. The ability of the human body to store excess food as fat kept our ancestors alive through lean times, and being able to easily lose weight was not a helpful characteristic for those ancestors. In our modern world of grocery stores and fast food, genes that helped our ancestors might make it hard for us to lose weight if we want to.

Psychological/Behavioral Influences

When your mouth waters in response to the smell of a roasting Thanksgiving turkey and steaming hot pies, you are experiencing a psychological influence on food intake. Pleasant smells and tastes influence what and how much we eat. Mood and emotions are associated with food intake. Depression, low self-esteem, compulsive disorders, and emotional trauma can influence food intake and body weight.

Habits and behaviors also influence food intake. Habits associated with high food intake include

  • Choosing large serving sizes
  • Frequent snacking on salty foods
  • High television and computer use
  • Frequent eating outside the home

A study of patrons of an all-you-can-eat buffet linked behaviors during a meal to an increased risk of obesity. Choices associated with obesity included using a larger plate, sitting facing the buffet, using a fork instead of chopsticks, beginning to eat quickly instead of browsing the entire buffet first, and even leaving a napkin on the table instead of putting it on the lap.[4] Studies such as this show correlations and not cause-and-effect relationships, but they illustrate the complexity of human eating behaviors. It is possible that paying attention to habits and behaviors could help curb the obesity epidemic.

Societal Influences

Society affects what and how much we eat. Portion sizes have increased dramatically in the past few decades. For example, a bagel is now more than twice the size it was in the 1960s. Today, Americans have easy access to calorie-dense foods and beverages, which is a large contributor to the rapid increase in overweight and obesity. Sub-cultures within the United States have traditionally had different eating habits, but changes in eating habits have had impacts. For instance, Native Hawaiians and Pacific Islanders who have adopted the standard American diet over traditional diets rich in fruits, vegetables, and fish now share the increase in obesity.

The fast-food industry supplies Americans with a large proportion of their diet and impacts the workings of the entire food system. Many popular fast-food items have little nutritional value, are highly processed, and are rich in saturated fat, salt, and added sugars. In 2015, Americans spent over $200 billion on fast food, up from $6 billion in the early 1970s.[5] The fast-food business is likely to continue to grow worldwide, and it is unrealistic think that people will stop eating easily-available, tasty, supposedly inexpensive food. One idea to improve health is to increase the availability of nutrient-dense whole foods in the fast-food industry. Consumer choices will increase healthier offerings; foods available at restaurants such as Subway and McDonald’s illustrate this trend. It is possible that engaging the fast-food industry in serving healthier foods could improve the American diet.

Tools for Change

Support the consumer movement of encouraging the fast-food industry and your favorite local restaurants to serving more nutrient-dense foods. You can begin this task by starting simple, such as requesting extra tomatoes and lettuce on your burger and more nutrient-dense choices in the salad bar. Also, choose their low-calorie menu options and help support the emerging market of healthier choices in the fast-food industry. When you do need a quick bite on the run, choose restaurants that serve healthier foods. Ask for nutrition information about foods so the restaurant becomes more aware that their patrons are conscious of nutrition issues.

References

  1. Wolf G, Miller NE. Lateral hypothalamic lesions: Effects on drinking elicited by carbachol in preoptic area and posterior hypothalamus. Science, 1964: 143, 585–587. https://www.ncbi.nlm.nih.gov/pubmed/14080328 Accessed October 2, 2024.
  2. Dardeno TA, Chou, SH, et al. Leptin in Human Physiology and Therapeutics. Front Neuroendocrinol. 2010; 31(3), 377–93. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2916735/?tool=pubmed. Accessed September 22, 2017.
  3. Levin BE. Developmental Gene X Environment Interactions Affecting Systems Regulating Energy Homeostasis and Obesity. Front Neuroendocrinol. 2010; 3, 270–83. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2903638/?tool=pubmed. Accessed September 22, 2017.
  4. Brian Wansink B and Payne CR. Eating Behavior and Obesity at Chinese Buffets. Obesity, 2008: 16, 1957–1960. doi:10.1038/oby.2008.286. Published online 5 June 2008. https://onlinelibrary.wiley.com/doi/epdf/10.1038/oby.2008.286. Accessed March 5, 2021.
  5. Sena, M. Fast Food Industry Analysis 2020 – Cost & Trends. Franchise Help, 2021. https://www.franchisehelp.com/industry-reports/fast-food-industry-analysis-2020-cost-trends/ . Accessed March 5, 2021.

Attributions

Adapted by Pattie S. Green, Ph.D. and Jonathan E. Pottle, Ph.D., Tacoma Community College, from the following sources:

License

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Introduction to Human Nutrition: A Textbook for Tacoma Community College Students Copyright © 2026 by Pattie S. Green and Jonathan E. Pottle, Tacoma Community College is licensed under a Creative Commons Attribution 4.0 International License, except where otherwise noted.