Hunger, Eating, and Health Lecture Slides PDF

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HelpfulHawk

Uploaded by HelpfulHawk

Brock University

2025

Charlis Raineki

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eating disorders obesity hunger physiology

Summary

This document presents lecture slides from Brock University, covering the topics of hunger, eating, and health. It delves into energy metabolism, hormonal control, and the factors that regulate food intake, including the hypothalamus and set point theory. The slides also explore obesity, its causes, and potential treatments.

Full Transcript

Hunger, Eating, and Health PSYC/NEUR 2P37 Charlis Raineki, PhD (he/him) January 30, 2025 Learning Objectives - Describe the process of digestion and the 3 phases of energy metabolism - Discuss the theories of hunger and the factors that in...

Hunger, Eating, and Health PSYC/NEUR 2P37 Charlis Raineki, PhD (he/him) January 30, 2025 Learning Objectives - Describe the process of digestion and the 3 phases of energy metabolism - Discuss the theories of hunger and the factors that influence eating - Evaluate the concept of hypothalamic hunger and satiety centers - Discuss obesity, its causes, and treatments Why do we eat? - Biological perspective - To obtain energy we need to support our everyday activities - To rebuild cells and manufacture various hormones, chemicals, and enzymes - Ultimately to promote survival - Social and psychological perspective - To socialize - To celebrate - Form friendships, reaffirm relationships and commitments - Stress Hunger and satiety - Two competing behavioral states - Hunger – desire for food - Satiety – sense of fullness (or satisfaction) Hunger Satiety - Complex mechanisms that anticipate future requirements Source of energy - Carbohydrates (starches and sugars) - Broken down into glucose, fructose, and galactose (monosaccharides) - Immediate source of energy - body will burn glucose first - Excess glucose can be stored in the liver and muscles - Fats (meats, milk products, seeds/grains) - Broken down into fatty acids - Immediate source of energy - Excess can be stored in fat tissue - Proteins (meats, beans, nuts, seeds) - Broken down into amino acids - May be turned into glucose, glycogen, or fat depending on needs - Used in the body for growth, repair, and energy Energy metabolism Three phases - Cephalic - Preparation to eat - Absorptive - Energy absorbed - Fasting - Withdrawing energy from reserves Copyright © 2021, 2018, 2014 Pearson Education, Inc. All rights reserved. Hormonal Control of Energy Balance Insulin & Glucagon - Insulin - Enables glucose to enter the cells (not in neurons) - Promotes the use of glucose as source of energy - Stimulates the production of glycogen, proteins and fat - Stimulates the storage of glycogen, proteins and fat - Glucagon - Stimulates glycogen breakdown - Promotes the release of free fatty acids from adipose tissue - Stimulates the conversion of free fatty acids to ketones Insulin and glucagon roles Learning Objectives - Describe the process of digestion and the 3 phases of energy metabolism - Discuss the theories of hunger and the factors that influence eating - Evaluate the concept of hypothalamic hunger and satiety centers - Discuss obesity, its causes, and treatments Theory of hunger: Set point - Hunger a consequence of an energy deficit - Each individual has an optimal level of energy resources – set point set point - Body seeks to return to this set point – homeostasis Copyright © 2021, 2018, 2014 Pearson Education, Inc. All rights reserved. Set point theory – What is monitored? - Glucostatic theory - Glucose levels determine when we eat - Lipostatic theory - lipo think liposuction - Fat stores determine how much we eat over long term - Explain how body weight tends to be constant over time - Long-term regulation Theory of hunger: Positive-incentive perspective - Anticipated pleasure - Animals driven to eat by the expected pleasure of eating - Expected pleasure = positive-incentive value (hedonic value) - Craving - Eating (and the perception of hunger) is initiated by craving - Enables you to take advantage of good food (when it’s available) - Multiple factors influence hunger - Flavor of the food - Knowledge about the food (learning) - Time since last meal, amount of food in gut, blood glucose Factors that determine what we eat - Innate preferences - Evolutionarily driven - Naturally preferred - Sweet and fatty foods – high-energy foods - Salty food – sodium-rich - Naturally avoided - Bitter tastes – associated with toxins Factors that determine what we eat - Learned taste preference and avoidance Training Test Flavour A → Glucose Flavour A vs. Flavour B Flavour B → Water Rats PREFER Flavour A Training Test Flavour A → LiCl Flavour A vs. Flavour B Flavour B → Water Rats AVOID Flavour A Factors that determine what we eat tasted the monarch and then spit it out cause it was nasty to them - Learned taste preference and avoidance - Blue jays and monarch butterflies Factors that determine what we eat essentially 2 rats were in the same room, one was taken away it ate cinnamon the other rat smelled it - Learned taste preference and avoidance on the other one breath and decides to eat the cinnamon after - Social transmission of food preference Modified from Shettleworth, 1998 Factors that determine what we eat the study suggest that animal have the ability to choose food that will complete their diet - Nutritional content - Sodium deficiency induces innate drive to consume salty foods - Associating salt with flavors Training Injection Test Almond + Salt Nothing Prefer banana solution Banana + Sugar Formalin Prefer almond solution - Other vitamin and mineral deficiencies must be learned since taste is not obvious - Thyamine (vitamin B1) depleted rats learn to choose a complete diet when offered 2 choices – effect weakened when there were 10 choices Factors that determine when we eat - Most mammals will eat many small meals throughout the day - With modern lifestyle, we eat fewer large meals - Family, daily routines, schedules - Premeal hunger - Eating a meal stresses the body: Influx of fuel moves it away from homeostasis - Signals for a meal (e.g., time of day, smells) evoke a cephalic phase - Insulin releases into blood → decreases blood glucose Factors that determine how much we eat - Satiety signals Plays a major role in how much we eat - Food in the gut - Glucose in the blood - Appetizer effect - Small amount of food may increase hunger - Serving size - The larger the serving, generally the more consumed Factors that determine how much we eat - Social influences - Even rats eat more in a group Factors that determine how much we eat - Sensory-specific satiety - More tastes available can lead to more eating – cafeteria diet Martire et al., 2013 - Satiety is sensory-specific it becomes less enjoyable - As you eat one type of food the positive-incentive value of the food decreases, but if offered a different food, you will eat again Learning Objectives - Describe the process of digestion and the 3 phases of energy metabolism - Discuss the theories of hunger and the factors that influence eating - Evaluate the concept of hypothalamic hunger and satiety centers - Discuss obesity, its causes, and treatments Functions of the Maintenance of homeostasis hypothalamus Influences on emotional, motivational, and affective aspects of behavior through links with the limbic system Regulation of food intake, body weight, electrolyte balance, body temperature, reproduction, sleep- wake cycle, and circadian rhythms Regulates endocrine function through the hypothalamic-pituitary system Regulation of food intake, body weight, electrolyte balance, body temperature, reproduction, sleep- Functions of the wake cycle, and circadian rhythms hypothalamus Regulates endocrine function through the hypothalamic-pituitary system - No single brain region has control of appetite, but the hypothalamus is important for regulation of: - Food intake - Metabolic rate - Body weight Overview of the hypothalamic nuclei Krebs et al.: Lippincott’s Illustrated Reviews of Neuroscience Copyright LWW 2011 Satiety center Hypothalamic hunger and it turned out to be wrong satiety centers - A dual-center hypothesis proposed two centers in the hypothalamus - One for signaling satiety Hunger center - Ventromedial hypothalamus (VMH) venni arent you full - One for signaling hunger - Lateral hypothalamus (LH) im literally hungy Ventromedial hypothalamus The satiety center - Ventromedial hypothalamus (VMH) lesions cause animals to eat to excess (hyperphagia) and become obese, suggesting the VMH could be a satiety center - Two phases constant - Dynamic phase: change - Excessive eating, weight gain - Static phase: - Body weight maintained over time Copyright © 2021, 2018, 2014 Pearson Education, Inc. All rights reserved. Problems with the VMH as the satiety center - Damage limited to the VMH does not consistently increase eating - Large VMH lesions also affect the ventral noradrenergic bundle that projects to the paraventricular nuclei (PVN) - Bilateral lesion of the ventral noradrenergic bundle produces hyperphagia and obesity as well - Bilateral lesion of the VMH increases blood insulin levels - Increases lipogenesis (production of fat) - Decreases lipolysis (breakdown of body fat) Thus, rats must consume more calories to meet demand Lateral hypothalamus The hunger center - Lateral hypothalamus (LH) lesions cause aphagia (refusal to eat), suggesting LH is a hunger center Copyright © 2021, 2018, 2014 Pearson Education, Inc. Copyright © Cengage Learning 2016 All rights reserved. Problems with the LH as the hunger center - The aphagia (refusal to eat) may be due to lack of responsiveness to sensory input, such as food and water - Possible motor disturbance - However, - Specific lesion of LH cell bodies (sparing passing fibers) resulted in major loss of feeding with out loss of arousal and activity Changes in body weight after hypothalamic lesion Arcuate nucleus of the hypothalamus: The appetite center - Neurons of the arcuate nucleus are sensitive to hunger and satiety signals - Leptin - Ghrelin - Peptide YY3-36 (PYY3-36) - Insulin state of satiety Leptin - Discovered in mice with a mutation in the obese (ob) gene - ob/ob mice have more fat cells than wild-type - ob/ob mice become obese - Even when offered an unpalatable diet or when required to work hard to obtain food - ob/ob mice do not produce leptin Leptin is a hormone that helps regulate body weight, hunger, and fat storage - Leptin is produced by fat cells (adipocytes) - Low levels of leptin increase hunger and decrease physical activity - High levels of leptin decrease hunger and increase physical activity - Long-term regulation of feeding behavior Leptin - Patient with congenital leptin deficiency shows a similar phenotype to ob/ob mice - Treatment with the leptin result in normalization of the body weight - Before treatment - 3 years old - 42 Kg - After treatment - 7 years old - 32 Kg Farooqi and O’Rahilly, 2014 Ghrelin Ghrelin is a hormone that increases appetite and food intake. It's often called the "hunger hormone" because it signals the brain when the stomach is empty - Produced by endocrine cells in the stomach - Potent appetite stimulant - Ghrelin levels rise during fasting - Trigger stomach contractions - Ghrelin levels drop after a meal - Obese subjects have lower baseline levels of ghrelin than lean subjects prior to eating, but levels do not drop after a meal Peptide YY3-36 (PYY3-36) - Produced by cells in the small and large intestine - Potent appetite suppressant - PYY3-36 blood levels are low prior to eating - PYY3-36 levels rapidly raise during a meal - Lower than average levels of PYY3-36 are associated with obesity - Post-meal increases of PYY3-36 in normal weight people are associated with feelings of satiety - NPY: neuropeptide Y - AgRP: agouti-related peptide Integration of the hormonal - - POMC: pro-opiomelanocortin CART: cocaine- and amphetamine- regulated transcript signals in the hypothalamus - Two sets of neurons in the arcuate - NPY/AgRP neurons – stimulate appetite - POMC/CART neurons – inhibit appetite - Lateral hypothalamus - POMC/CART neurons → release melanocortin in LH - NPY/AgRP neurons → release AgRP in LH - Paraventricular nucleus - NPY/AgRP neurons → release NPY in PVN Learning Objectives - Describe the process of digestion and the 3 phases of energy metabolism - Discuss the theories of hunger and the factors that influence eating - Evaluate the concept of hypothalamic hunger and satiety centers - Discuss obesity, its causes, and treatments Rates of obesity over the years Data from OECD Why is there an epidemic of obesity? - Evolution favored individuals that - Preferred high-calorie food - Ate to capacity - Stored as much energy as possible Copyright © 2011 Pearson Education, Inc. - Modern lifestyle - Decline of home cooking - Larger portions, junk food - TV, internet, video games… - Lack of physical activity Illustration by Nicola Jennings Why do some - Energy input differences - Craving for high-calorie foods people become - Cultural norms obese while others - Large cephalic-phase response to sight and smell of food do not? - Energy output differences - Exercise - Basal metabolic rate - Diet-induced thermogenesis - Genetics interact with body energy input and output Treatment of obesity: Semaglutide - Glucagon-like peptide-1 (GLP-1) analogue - GLP-1 stimulates insulin and inhibits glucagon - Reducing blood glucose levels Treatment of obesity: Semaglutide - Clinical trial results Blundell et al., 2017 Treatment of obesity: Semaglutide - Clinical trial results Blundell et al., 2017 Gastric bypass Treatment of obesity: Bariatric surgery - Treatment indicated only for extreme obesity - Two different procedures mostly used Gastric band Copyright © 2021, 2018, 2014 Pearson Education, Inc. All rights reserved. Puzziferri et al., 2014 Treatment of obesity: Bariatric surgery in Canada Learning Objectives - Describe the process of digestion and the 3 phases of energy metabolism - Discuss the theories of hunger and the factors that influence eating - Evaluate the concept of hypothalamic hunger and satiety centers - Discuss obesity, its causes, and treatments

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