Hunger and Eating_2022_StudentUpload.pptx

Biological Psychology of Hunger and Eating Biopsychology Lecture 7 Blair Saunders READ CHAPTER 12 OF TEXTBOOK Eating is one of the fundamental biological drives on the planet Why do we eat? Energy Food supplies energy in the form of glucose, fats, protein, and glycogen These energy sources are central the functioning of most biological systems For example, the energy from food fuels: • Growth and development • Brain activity (glucose) • Muscle movements • Thermoregulation Why do we eat? Eating also supplies the body with the key ingredients required to survive and function (e.g., vitamins, minerals, amino acids, sugars, fats etc.). What we eat is a key determinant of health! Why do we eat? Eating is also highly pleasurable, social, cultural, familyoriented And the fun part of food seems to have got us into a spot of bother Today’s goals Overall objective: To understand the psychology and biology of hunger and eating, and how these processes relate to weight management Theme 1: The function and digestion of food What is the purpose of eating? How do we digest food? How is the energy from food stored and used by the body? Theme 2: Theories of hunger What psychological and biological factors make us hungry? How do we know when we are full? What theories best describe hunger and satiety? Theme 3: Body Weight Regulation What psychological and biological factors contribute to body weight? Why are some people obese, while others are not? What are the biological effects of restricted diets, and why are diets so ineffective? Biological Psychology of Hunger and Eating Part 1: Hunger and satiety Blair Saunders The gastrointestinal tract Energy Storage Digestion delivers energy to the body in three forms - Lipids (fats) Amino acids (used to build protein) Glucose (Carbs & Sugar) Our bodies need energy all the time, but we only eat intermittently. Acting like a battery, our bodies stores fat, protein, and glycogen to use as energy when food is not in immediate supply. Our primary source of energy storage is in our adipose (fat) tissue. Energy Metabolism Energy metabolism refers to the chemical processes through which energy is used and made available for bodily functions. Metabolism is largely controlled by the circulation of 2 key pancreatic peptides that act as a hormones: Insulin  Use of glucose as primary energy source  Conversion of blood glucose to glycogen & fat, and amino acids to proteins  Storage of energy (more fat in adipose tissue, proteins in muscle, glycogen in liver and muscle) Insulin increases the short-term use and long-term storage of glucose. Insulin is used at times when glucose levels are (or are expected to be) high Glucagon  Release of free fatty acids from adipose tissue (fat reserves) to provide energy to the body  Gluconeogenesis: The conversion of protein to glucose to use a fuel Glucagon withdraws energy from the body’s reserved when glucose is not available Glucagon is used at times when glucose levels are low Phases of Energy Metabolism Energy metabolism is dynamic, and changes over three phases that are related to the recency of food consumption How might the hormones insulin and glucagon aid metabolism during these phases? Starts with sight, smell, or thought of food. Ends when food enters bloodstream CEPHALIC PHASE The period in which energy is absorbed into bloodstream. ABSORPTIVE PHASE The burger is in the distant past. Immediate metabolic effect of food no longer meets energy requirements. Energy must be extracted from reserves FASTING PHASE Theme 2: Theories of hunger What determines feeling hungry versus feeling full? Hunger might determine what, when, and how much we eat What is hunger anyway? “Craving” “Desire” Is hunger a motivational state? “Lack of food” Is hunger caused by the depletion of energy reserves? Idea 2: Theories of Hunger, or, what governs how much we eat? What is satiety anyway? Thinking about a viable scientific theory of hunger Hunger and eating are incredibly complex behaviours. What must a model of hunger explain? Hunger can be brought about by a range of perceptual, cognitive, and social factors (e.g., the smell of food, imagining a chocolate bar, the behaviour of your friends). So a viable theory of hunger must be flexible enough to deal with the broad range of factors that influence hunger, including: • Current energy needs • Desires for the appropriate vitamins and minerals • The influence of pleasure and taste preference on food • The influence of social and cultural factors on eating • Current levels of obesity Theme 2: Two theories of hunger 1) Set-point theory 2) Positive-Incentive Perspective Set-point theory Basic premise: • • • • Hunger arises when people are experiencing an energy deficit. Eating replenishes energy reserves to some optimal set-point, and hunger is alleviated. Set-point theory is a negative feedback system Questions: What is this hypothetical energy source? Is it glucose, fat, protein, something else? Evaluating set-point theory: PROs Intuitive appeal When we are hungry, we feel like we are out of energy, and that we have to replenish some reserve Simplicity Set-point theory proposes a simple homeostatic model through which hunger is regulated. Occam’s razor stresses parsimony. We should accept the simplest theory or model that can explain the phenomenon. Do you think that set-point theory is a good model of hunger? Positive Incentive Perspective (Berridge, 2004) Humans and animals are drawn to eating for foods pleasurable quality, rather than because they are running out of immediate resources Positive Incentive Perspective (Berridge, 2004) Based on motivational accounts of affect/emotion Anticipated positive experience Engaging in behaviours that help us survive Eating Sex Socialising Sleeping Pleasure from food Sweet tastes produce liking responses across species (Berridge, 2004) Pleasure from food Sweet tastes produce liking responses across species, while bitter tastes produce aversive responses (Berridge, 2004) Evolutionary Perspective: Pleasure-incentive perspective Wait… surely we don’t just eat to have fun?? Overeating is killing people, so why would we ever evolve to behave like this?? Positive-incentive theory: PROs Positive-incentive perspective suggests that hunger and cravings depend on the interaction of multiple factors that influence the positive incentive value of food: • • • • • • The taste of the food Your previous experience with the food Sensory feedback about the amount of food in your gut The presence of absence of other people in the eating context Your current mood Your current glucose levels, and so on… Unlike set-point theory, the positive-incentive perspective does not limit hunger to one single mechanism. Class exercise: Show me the evidence!! We will now explore the factors that govern what we eat, how much we eat, and when we eat. Exercise: Keep a tally of evidence that is better explained by set-point theory, the positive-incentive perspective, or both. What we eat? Innate taste preferences and aversions Its important that we have some system of preferences that allow us to select the most appropriate foods to eat. Hunger can steer us towards the energy and nutrition that we need Innate taste preferences Sweet and Fatty tastes Adaptive: These foods tend to be characteristic of high-energy, high nutrition foods Salty tastes Adaptive: characteristic of sodium rich foods. Sodium regulates fluid balance, nervous system activity Innate taste aversions Bitter tastes In nature, bitter tastes are often coincide with poisonous plants How do we know when we are full? Set-point hypothesis: Signals about the energy content from the food eaten returns us to a pre-defined energy requirement. Positive-Incentive hypothesis: We should stop eating when food is no longer pleasurable. How much we eat: Sham eating Meal 1 after surgery: What would set-point theory predict to happen here? Thinking more about satiety Appetizer effect After you have a small amount of food, do you feel like eating more or less? Serving Size and Satiety People tend to eat more if they are given large portions Social Influences and Satiety People tend to eat more when they are in the company of others than when they are alone. Lab rats also eat more in groups. Are these effects consistent with set-point theory or positive incentive theory? Does eating lead to a general feeling of fullness? Or do we only feel full for the food we have just eaten? Cafeteria Diet Cafeteria Diet: A diet where you are offered multiple different tastes to sample from (e.g., hotdogs, fizzy drinks, fries, cakes, candy). Rogers & Blundell (1980) • Group 1: Rats allowed to freely eat normal foods • Group 2: Rats in an environment with access to multiple highly palatable foods (bread and chocolate) and normal food + = Rats offered bread and chocolate in addition to their everyday foods consume 89% more calories and gain 49% in bodyweight versus other free feeding rats Sensory Specific Satiety • • • • Eating one food  reduced positive incentive value for all food in general AND a massive reduction in incentive for the food that you just ate Once you stop eating one food (e.g., Pizza), you will still see some value in eating another (e.g., ice cream) Overall Idea: Satiation is category specific—you might satiate on savoury foods, but still have room left for something sweet Sensory Specific Satiety: Human Evidence Rolls et al. 1981 (Experiment 2): Step 1 • • • Ps rate pleasantness of 8 foods Then given one of these foods to eat for lunch (either sausage or cheese on crackers) Eat this food until full Step 2 • • Re-rate foods after eating. Rate both how much they like the food, and how much they would like to eat more Why might it be adaptive for our appetites to work like this? Sensory Specific Satiety: Cafeteria Diet Booth (1981) Explored the time-course of sensory specific satiation Category specific satiation was observed soon after eating a specific food Reduced appetite for all food categories was observed after approximately 30 minutes after eating Slower ingestion of food produces a more wide-scale reduction in appetite Break Time DON’T FORGET TO SIGN THE REGISTER Biological Psychology of Hunger and Eating Part 2: Physiology of satiety and body weight regulation Blair Saunders The physiological correlates of hunger and satiety Do blood glucose levels regulate hunger and satiety? Step point idea: glucose = body fuel So do we monitor circulating glucose and feel hungry when blood glucose levels are low, and satiated when glucose levels are high? Do blood glucose levels regulate hunger and satiety? Campfield & Smith (1990) • • Rats housed with free access to food & water Circulating levels of blood glucose continuously monitored Findings • • Baseline blood-glucose levels barely fluctuates > 2% 10 minutes before feeding, glucose levels drop > 10% Later results • • Elimination of glucose dip does not eliminate eating behaviour Missing an expected meal results in recovery of glucose levels without influx of new food Conclusion Initiating eating actually controls glucose levels, rather than glucose levels initiating eating Hypothalamic Hunger and Satiety Centres Remember back to Elaine’s lectures Located in the “limbic system” underneath the thalamus Receives inputs from a number of hormones and peptides Associated with the regulation of a number of hormonal and metabolic processes Hypothalamic Hunger and Satiety Centres: The view in the 1940s Ventromedial Hypothalamus • • • Lesions caused excessive eating (hyperphagia) Dynamic Phase: In the weeks after surgery the animal eats excessively and gains weight rapidly Static Phase: Food intake reduces to a level that is sufficient to maintain this increase in weight Lateral Hypothalmus • • • Lesions result in the animal stopping eating (aphagia) Animals also stop drinking water Animals have to be tube fed to stay alive These studies led to the conclusion that the hypothalamus has distinct feeding and satiety regions However, these conclusions were wrong! Lesions to the ventromedial hypothalamus (the “eating” area)  increased blood concentration of insulin Suggests hypothalamus plays a role in regulating hormones Why might insulin make the rats increase stores of fat? Insulin  Use of glucose as primary energy source  Conversion of blood glucose to glycogen & fat, and amino acids to proteins  Storage of energy (more fat in adipose tissue, proteins in muscle, glycogen in liver and muscle) So rats with lesions to the ventromedial hypothalamus ate more to fuel the increased conversion of glucose to fat caused by insulin levels. The older studies got the causality the wrong way around! Could the same metabolic effects also explain some portion of obesity in humans? A role for the gastrointestinal tract in satiety Gastrointestinal tract refers to the collection of organs that digests food and produces faeces Question: Do signals from the gastrointestinal tract—such as feelings of a full stomach— regulate hunger and satiety? Seems to jive with our intuitions. We often talk about our “full” or “bursting” stomachs after a meal A role for the gastrointestinal tract in satiety Cannon and Washburn (1912) Cannon was a brilliant scientist… …Washburn could swallow a balloon The results are a little consistent with a set-point theory. This time with the set-point being stomach capacity Criticism: A role for the gastrointestinal tract in satiety Gastrectomy – surgical removal of the stomach. Interestingly, people who have their stomachs removed entirely still show signs of hunger and satiety. Hunger and satiety signals from the stomach Koopmans (1981) Implanted second stomach attached to circulatory system, but not the nervous system Eating behaviours were related to the calories in the injected food Why would this happen if the stomach is not connected to the brain by the nervous system? Hunger and satiety peptides Peptides are short chains of amino acids (similar to proteins) that act as hormones and neurotransmitters Ingestion of food interacts with receptors in the gastrointestinal tract and releases peptides into the bloodstream Many peptides have been associated with hunger and satiety: • Cholecystokinin (intestine) • Insulin (pancreas) • Ghrelin (stomach) • Leptin (fat) Suggests that many factors determine hunger and satiety Theme 3: Body weight & Health What factors control our body weight? (i.e., how much energy is stored in our fat or protein). Why do people become overweight? Three common theories: 1. Willpower/conventional wisdom. • • Overweight people should resist eating unhealthy snacks and get more exercise Idea associated with stigma 2. Lifestyle/environmental factors • We live in an obesogenic environment. High access to unhealthy foods makes people more likely to become overweight 3. Biological/Genetic factors • Metabolism and genetic factors drives our body weight, and also how much we eat What do you think it most important? Set-point theory of body weight. Set-point theory of body weight. • Idea that our weight levels are very rigid and largely pre-determined by our genes. They don’t fluctuate much from month to month, or year to year. • People should be healthy when they are at or around their natural set point. What evidence is there for a natural set point? A genetic basis of body weight? Evidence from twin studies, from twins brought up in the same household environment Identical (Monozygotic) twins: same genetics and environment Fraternal (Dizygotic) twins: same genetic resemblance as regular siblings and same environment Vermont Prison Study Ethan Sims in 1960s Endocrinologist interested in the effects of overeating on fat cells Step 1: Raise food consumption to 4000 cals/day • People gained some weight initially, but it tapered off Step 2: Raise food consumption to 10000 calories/day • • 4-6 months for people to increase body weight by 20%. It also plateaued Metabolism increased by 50% Weight rapidly returned to pre-diet levels (i.e., set-point) after normal diets resumed What metabolic processes counteract food intake The body in part controls fat levels by changing the efficiency with which it metabolises energy Mechanisms: 1) Diet-induced thermogenesis 2) Basal metabolic rate (resting energy metabolism) • Higher levels of either of these mechanisms reduces the fattening effects of food intake • This allows the body to maintain stable fat reserves • Factor also makes it very Do specific genes determine your set-point? Set-point theory leads to the suggestion that their might be specific genes that partially determine how our body will metabolise and store energy 1950s: Spontaneous genetic mutation at Jackson Laboratory in Maine produced mice that ate more and stored more adipose tissue than normal laboratory mice These mice receive two copies of a gene that was called “Obese” (ob), and are referred to as ob/ob mice Leptin and ob/ob mice Ob/ob mice have reduced production of a peptide called Leptin (from the Greek Leptos, “thin”). Leptin seems to serve as an afferent signal in a homeostatic negative feedback loop allowing us to maintain stable fat levels Friedman (2010), Nature Medicine HOMEWORK EXCERCISE So, have we cured obesity? Later studies failed to replicate this effect. It’s complicated More than 100 human chromosomes have been linked to obesity. Obesity could be caused by a number of different things But we talked about set-point theories of hunger before, and decided it was wrong??!! Set-point theory of body weight. Set-point theory of body weight. • Idea that our weight levels are very rigid and largely pre-determined by our genes. They don’t fluctuate much from month to month, or year to year. • People should be healthy when they are at or around their natural set point. What evidence is there for a natural set point? Set-point theory of weight has some serious drawbacks Foremost, this theory fails to account for the fluctuations in weight that people seem to go through over the course of their lives. Settling-point theory This idea is proposed as a more flexible alternative to setpoint theory Body weight varies around a “settling point”, rather than a fixed weight range Body finds natural equilibrium that is defended by metabolic changes if fat levels increase rapidly Body weight is stable unless there are large and enduring changes in the factors that disturb homeostasis: • Food availability and quantity • Perceived incentive value of food • Changes in lifestyle • Changes in metabolism (e.g., from gaining muscle) Obesity and Health Health Cross-sectional evidence from the Japanese Island of Okinawa Okinawa study (Kagawa, 1978) • • Inhabitants consume 20% fewer calories on average than other adult Japanese people Okinawan School children eat 38% bellow recommendations But • • Mortality rates lower in Okinawa than other parts of Japan Death rates from stroke, cancer, and heart disease were much lower than in the rest of Japan Correlation warning Experimental Evidence Weindruch et al. (1986) Conducted a study of food deprivation in laboratory rats All reductions in food intake from free-feeding resulted in improved health and greater longevity Rats in group 4 had: • Lowest risk of cancer • Best immune system responses • Greatest maximum life span Suggests that fasting might be a way to improve health Group 1 (Free Feeding) Group 3 (55%) Group 2 (25%) Group 4 (65%) This is getting quite depressing Body weight, as we have learned, is very hard to regulate Remember: changing your body weight is not the only way that you can become healthier Matheson et al. (2012) Examined the association between healthy lifestyle habits and mortality in as sample of 11,761 men and women across varying weight levels 5-a-day? Moderation? Exercise? Smoking? Healthy habits and obesity 5-a-day? Matheson et al. (2012) Moderatio n? Exercise? Smoking? Healthy habits and obesity 5-a-day? Matheson et al. (2012) Moderatio n? Exercise? Smoking? Healthy habits and obesity 5-a-day? Matheson et al. (2012) Moderatio n? Exercise? Smoking? Healthy habits and obesity 5-a-day? Matheson et al. (2012) Moderatio n? Exercise? Smoking? Summary • Hunger and satiety are explained by both set-point and positive-incentive perspectives. Which is correct? • Appreciate the range of psychological and physiological factors that might determine feelings of hunger and satiety • Realize that body-weight is not a simple factor of calories consumed. The body can work to maintain a stable body weight against sudden increases/decreases in calories • Understand the impact of calorie restriction on health, but also appreciate the difficulty of regulating body weight and appreciate that health is the result of many health promoting behaviours. References Pinel & Barnes (2014). Introduction to Biopsychology (Chapter 12) Friedman, J. M. (2010). A tale of two hormones. Nature Medicine, 16, 1100-1106. Mann, T., Tomiyama, A. J., Westling, E., Lew, A. M., Samuels, B., & Chatman, J. (2007). Medicare's search for effective obesity treatments: diets are not the answer. American Psychologist Matheson, E. M., King, D. E., & Everett, C. J. (2012). Healthy lifestyle habits and mortality in overweight and obese individuals. The Journal of the American Board of Family Medicine If you are interested

Hunger and Eating_2022_StudentUpload.pptx

Related

Transcript

Upgrade to continue