Module 1 Hunger - PDF

PHYSIOLOGICAL/BIOLOGICAL PSYCHOLOGY Kalat, J. W. (2019). Biological Psychology 13th Edition. Boston, MA, USA: Cengage Module: INTERNAL REGULATION Major Topics: 1. Temperature Regulation 2. Thirst 3. Hunger Module 1: Hunger Digestion and Food Selection - Digestion is the process...

PHYSIOLOGICAL/BIOLOGICAL PSYCHOLOGY Kalat, J. W. (2019). Biological Psychology 13th Edition. Boston, MA, USA: Cengage Module: INTERNAL REGULATION Major Topics: 1. Temperature Regulation 2. Thirst 3. Hunger Module 1: Hunger Digestion and Food Selection - Digestion is the process by which food is broken down into smaller molecules that cells can absorb and use for energy, growth, and repair. Understanding the digestive system and its mechanisms provides insight into how food is processed and how choices in food selection impact digestion and health. The Digestive Process 1. Mouth (Initial Stage) - Role in Digestion: Digestion begins in the mouth, where food is mechanically broken down by chewing. - Salivary Enzymes: Enzymes in saliva, such as amylase, begin breaking down carbohydrates into simpler sugars. This initial chemical digestion prepares food for further breakdown in the stomach. 2. Esophagus - Transportation:Once swallowed, the food (now called a bolus) travels down the esophagus through rhythmic muscle contractions known as peristalsis. The esophagus connects the mouth to the stomach. 3. Stomach Chemical Breakdown: - Food enters the stomach, where it mixes with hydrochloric acid and digestive enzymes, such as pepsin, which break down proteins. - The stomach's highly acidic environment kills bacteria and provides the optimal conditions for protein digestion.  Storage and Regulation: - The stomach temporarily stores food, releasing it gradually into the small intestine via the sphincter muscle at its base. 4. Small Intestine Primary Site of Digestion and Absorption: ○ The small intestine is the most crucial part of the digestive process, with specialized enzymes breaking down proteins, fats, and carbohydrates into their smallest components: Proteins → Amino acids Fats → Fatty acids and glycerol Carbohydrates → Simple sugars (e.g., glucose) ○ These molecules are absorbed through the walls of the small intestine into the bloodstream. Nutrient Distribution: ○ Blood carries the absorbed nutrients to the cells for immediate use or stores them for later. 5. Large Intestine Absorption of Water and Minerals: - The large intestine absorbs water from the remaining indigestible food matter, ensuring hydration and compacting the waste. - It also absorbs essential minerals, such as sodium and potassium. Excretion: - The leftover material is lubricated and prepared for elimination through the rectum and anus as feces. Food Selection and Its Impact on Digestion Food choices significantly affect how efficiently the digestive system functions: Carbohydrate-Rich Foods: ○ Complex carbohydrates, like whole grains, take longer to digest and provide sustained energy. ○ Simple sugars digest quickly but can cause spikes in blood sugar. Protein-Rich Foods: ○ Proteins from sources like meat, fish, and legumes require longer digestion in the stomach. ○ High-protein diets may strain the digestive system if not balanced with fiber-rich foods. Fats: ○ Fats are broken down slowly, providing long-term energy but potentially causing digestive discomfort if consumed in excess. ○ Healthy fats, such as those in nuts and avocados, support nutrient absorption. Fiber: ○ Dietary fiber, found in fruits, vegetables, and whole grains, enhances digestion by promoting bowel regularity and supporting the gut microbiome.  Hydration: ○ Adequate water intake is essential for efficient digestion and absorption, particularly in the small and large intestines. Part Primary Function Key Digestive Actions Mouth Begins Digestion Chewing, salivary enzyme action on carbohydrates Esophagus Transports food to stomach Peristalsis Stomach Breaks down proteins; stores Hydrochloric acid and enzyme food activity Small Intestine Digests and absorb nutrients Enzymatic digestion of macronutrients Large Intestine Absorbs water and minerals; Compacts waste, absorbs excretes waste water Consumption of Dairy Products The ability to consume dairy products as an adult is a fascinating example of evolutionary adaptation and genetic diversity among humans. It reflects how dietary needs and environmental pressures have shaped biological mechanisms in humans and other mammals. Milk Consumption in Mammals 1. Milk as the Initial Food Source: ○ For newborn mammals, milk is a primary food source, rich in nutrients necessary for growth and development. ○ During this phase, mammals produce lactase, an intestinal enzyme that breaks down lactose, the sugar found in milk, into glucose and galactose for absorption. 2. Weaning and Decline in Lactase: ○ As mammals mature and transition to solid foods, lactase production typically declines. ○ This decline appears to be an evolutionary mechanism to promote weaning and adapt to a diet more suited to adulthood. ○ Without sufficient lactase, consuming large amounts of milk can result in symptoms such as gas, stomach cramps, and diarrhea. Human Adaptations to Dairy Consumption Unlike most mammals, many humans maintain lactase production into adulthood—a phenomenon known as lactase persistence. However, this ability varies significantly across populations. 1. Prevalence of Lactase Persistence High Lactase Persistence: ○ Populations with a history of cattle domestication, such as in northern Europe and certain parts of Africa, have a high prevalence of lactase persistence. ○ For example, nearly all adults in northern Europe can digest lactose. Low Lactase Persistence: ○ In populations where cattle domestication and milk consumption were less common, such as in East Asia and some parts of Africa, lactase persistence is rare. ○ Nearly all adults in China and surrounding countries are lactose intolerant, as are many Native Americans and Indigenous Australians. 2. Evolutionary Adaptations The genetic ability to digest lactose in adulthood arose independently in different populations. ○ Europeans with lactase persistence typically share the same gene variant. ○ In Africa, several distinct genetic adaptations allow for lactase persistence, reflecting multiple instances of evolutionary convergence tied to the domestication of cattle. When cow’s milk became a dietary staple, selective pressure favored individuals who could digest lactose, conferring a survival advantage. 3. Lactose Intolerance and Alternatives Lactose Intolerance: ○ Individuals with low lactase levels may experience discomfort after consuming milk but can often tolerate fermented dairy products like cheese and yogurt because the fermentation process reduces lactose content. Dietary Adjustments: ○ Many lactose-intolerant individuals limit milk intake or switch to lactose-free or plant-based alternatives, such as almond, soy, or oat milk. Global Distribution of Lactase Persistence Europe: ○ Lactase persistence is highly prevalent in northern and western Europe but decreases in southern Europe. Africa: ○ The ability to digest lactose is patchy, with higher persistence in regions with a history of cattle herding, such as East Africa. Asia:  ○ Lactase persistence is rare in East Asia, where dairy consumption historically has been limited. Americas: ○ Lactase persistence in Native American populations is around 25%, while other groups reflect the ancestry of settlers or enslaved individuals. Implications for Modern Diets 1. Cultural Practices and Food Choices: ○ In regions where lactose intolerance is prevalent, diets traditionally exclude or minimize dairy products, focusing instead on alternatives like soy or coconut milk. 2. Health Considerations: ○ For those with lactose intolerance, dairy consumption must be managed to avoid digestive discomfort while ensuring sufficient intake of calcium and vitamin D from other sources. 3. Adaptation and Genetic Research: ○ The study of lactase persistence and lactose intolerance provides insights into human adaptation and evolution, highlighting the interplay between genetics, diet, and environment. Food Selection and Behavior The relationship between food selection and behavior is a topic of scientific interest, often surrounded by myths and misconceptions. Here's a closer look at how food choices impact behavior and cognitive functioning based on evidence: 1. Sugar and Hyperactivity The Myth: The belief that sugar causes hyperactivity in children is widespread, often reinforced by anecdotal observations during events like birthday parties or holidays. Scientific Evidence: Rigorous studies using controlled conditions, where children are given sugary and artificially sweetened snacks without knowing which is which, have consistently found no significant effect of sugar on: ○ Activity levels ○ Play behavior ○ School performance The belief persists likely due to confirmation bias, where people notice behavior that aligns with their expectations. For instance, a child's natural excitement at a party is attributed to sugar consumption rather than the social context or environmenturkey and Sleepiness** The Myth: It is often claimed that eating turkey causes sleepiness due to its content of tryptophan, an amino acid that the brain uses to produce serotonin and melatonin, chemicals involved in sleep regulation. Scientific Evidence: Turkey’s tryptophan levels: Turkey contains only an average amount of tryptophan, no more than other protein sources. Thanksgiving fatigue: The sleepiness commonly reported after Thanksgiving meals stems from overeating, which directs blood flow to the digestive system, leaving less for other activities. Carbohydrates and Tryptophan: Interestingly, eating a diet rich in carbohydrates can increase the brain’s uptake of tryptophan:  ○ Mechanism: Carbohydrates stimulate insulin release. Insulin reduces levels of competing amino acids, such as phenylalanine, by moving them into storage. This reduced competition allows more tryptophan to enter the brain, promoting sleepiness. ○ Conclusion: Dessert, rather than turkey, is more likely to cause drowsiness at a large meal. 3. Fish as Brain Food The Claim: Eating fish, particularly oily fish like salmon, improves cognitive functioning and supports brain health. Scientific Evidence: Rich in Omega-3 Fatty Acids: ○ Many fish are high in omega-3 fatty acids, particularly DHA (docosahexaenoic acid), which is crucial for brain development and function. Effects on Cognitive Development: ○ Mothers who consume significant amounts of seafood during pregnancy tend to have children who perform better on cognitive tests in infancy and later life. ○ Children benefit from the neuroprotective and developmental effects of omega-3 fatty acids. Protection Against Cognitive Decline: ○ Regular seafood consumption in older adults has been linked to slower cognitive decline, even among those with a genetic predisposition to dementia. Short- and Long-Term Regulation of Feeding Feeding regulation is a complex process involving multiple mechanisms and signals from various parts of the body. These signals ensure proper energy intake and satiety to maintain energy balance. Oral Factors 1. Role of Taste and Chewing: ○ Humans and animals have an inherent desire to taste and chew, even in the absence of hunger. ○ Evidence:  In an experiment, students consumed meals via a tube that bypassed taste and chewing. While they maintained a steady caloric intake, they found the experience unsatisfying and craved the sensory aspects of eating. In sham feeding experiments, animals with disconnected digestive tracts (food leaks out after swallowing) ate continually because the lack of nutrient absorption and stomach distension prevented satiety. 2. Key Insight: ○ Taste contributes to the eating experience but is insufficient for signaling satiety. Chewing and tasting without actual digestion does not fulfill the body’s need for nutrients. The Stomach and Intestines Stomach Distension Primary Signal for Satiety: ○ As the stomach stretches, it sends signals to the brain via the vagus nerve (cranial nerve X), indicating fullness. ○ Experimental Evidence: In animals with an inflatable cuff blocking food passage to the intestines, feeding stopped once the stomach was full, even though no digestion occurred. Duodenum's Role Nutrient Detection and Satiety Signals: ○ The duodenum, the first part of the small intestine, plays a critical role in satiety: 1. It absorbs nutrients and detects their type and quantity. 2. Contains taste-like receptors that inform the brain of food composition without conscious awareness. Hormone: Cholecystokinin (CCK): ○ Released by the duodenum in response to nutrient presence. ○ Functions: 1. Sphincter Constriction: CCK closes the muscle between the stomach and duodenum, keeping food in the stomach longer and promoting faster stomach distension. 2. Neural Signal Activation: CCK activates the vagus nerve, which signals the hypothalamus to release neurotransmitters that mimic CCK, amplifying the satiety response. Limitations of CCK in Weight Loss: While CCK can limit meal size, it only has short-term effects. Animals or humans compensate for smaller meals by eating more in subsequent meals, making it ineffective  for long-term weight loss strategies. Mechanism Signal or Role Outcome Oral factors Chewing and tasting provide Desire for sensory experience sensory satisfaction but are continues without digestion. insufficient for satiety. Stomach distension Stretching of the stomach Sufficient for satiety in most signals fullness via the vagus cases. nerve. Duodenum Nutrient detection and release Promotes meal termination of CCK enhance satiety by through dual mechanisms. affecting both digestion and neural signals. Cholecystokinin (CCK) Short-term signal to end a Limited to short-term meal meal by inducing stomach size regulation. fullness and stimulating hypothalamic pathways. Glucose, Insulin, and Glucagon The regulation of energy intake and blood glucose levels is a critical process involving several key hormones, particularly insulin and glucagon, which control the availability of glucose to cells: The Role of Insulin 1. During Meals: ○ Insulin is secreted by the pancreas in response to food intake. ○ It facilitates glucose entry into most cells, with the brain being an exception (brain cells take up glucose independently of insulin). ○ Excess glucose is stored in the liver as glycogen or in fat cells as fat. 2. After Meals: ○ Blood glucose levels gradually drop as glucose is stored and used by cells. ○ Reduced insulin levels slow the movement of glucose into cells, prompting hunger. 3. Prolonged High Insulin Levels: ○ In cases of constant high insulin (e.g., pre-hibernation in animals), glucose storage is excessive, leading to low blood glucose and increased hunger, causing overeating and fat accumulation. 4. Prolonged Low Insulin Levels (Diabetes): ○ Insufficient insulin means glucose remains in the bloodstream but cannot enter cells  efficiently, leaving them starved. ○ Symptoms include excessive hunger, weight loss, and excretion of unmetabolized glucose in urine. The Role of Glucagon Secreted by the pancreas when blood glucose levels drop, glucagon stimulates the liver to convert glycogen back into glucose, maintaining blood glucose levels during fasting periods. Leptin: Long-Term Regulation of Feeding Discovery of Leptin Researchers identified leptin, a hormone produced by fat cells, as a signal for fat reserves. Higher fat reserves lead to higher leptin levels, which inform the brain about the body's energy stores. Functions of Leptin 1. Energy Balance: ○ Low leptin signals depleted fat stores, prompting increased hunger and decreased activity to conserve energy. ○ Normal or high leptin levels reduce hunger and increase physical activity. 2. Puberty: ○ A sufficient leptin level is necessary for the onset of puberty, as it signals the body has enough energy reserves to support reproduction. 3. Activation of the Sympathetic Nervous System: ○ Leptin increases sympathetic activity, raising blood pressure and supporting energy regulation. Leptin Deficiency and Treatment 1. In Mice: ○ Mice without functional leptin become obese, inactive, and fail to reach puberty. ○ Leptin injections reverse these symptoms, reducing food intake and increasing activity. 2. In Humans: ○ Rare cases of leptin deficiency in humans can also be treated with leptin supplementation. Leptin Resistance  Most overweight people produce ample leptin, but their bodies may develop resistance to it, limiting its effectiveness in reducing appetite. Adding extra leptin has little impact on both overweight and normal-weight individuals, as beyond a threshold, leptin’s ability to suppress hunger is weak. Insights on Hunger and Satiety Mechanisms Short-Term Regulation: Insulin and glucagon manage meal-to-meal energy balance and blood glucose. Long-Term Regulation: Leptin adjusts for overall energy balance, preventing prolonged overeating or undereating. Evolutionary Implications Mechanisms promoting hunger are stronger than those ensuring satiety, reflecting an evolutionary adaptation to avoid starvation, which posed a greater survival risk than overeating in ancestral environments. The Lateral Hypothalamus (LH) The lateral hypothalamus plays a critical role in feeding behavior and integrating various sensory and physiological signals to control hunger. Its functions are multi-faceted, involving the control of taste responsiveness, hormonal signaling, and autonomic processes. It acts as a central hub, integrating signals from upstream brain regions, including the paraventricular nucleus (PVN). Functions of the Lateral Hypothalamus: 1. Taste Sensation and Appetite Regulation: ○ The LH communicates with the nucleus of the tractus solitarius (NTS), a part of the taste pathway, to enhance the taste of food during hunger. ○ This process involves altering the salivation response and increasing the perceived palatability of food. 2. Cortical Connections: ○ Axons from the LH extend into the cerebral cortex, which facilitates behaviors like ingestion and swallowing. The LH also enhances the sensory appeal of food (e.g., taste, smell, and sight). 3. Hormonal Influence: ○ The LH modulates the pituitary gland, promoting the secretion of insulin, which helps the body prepare for food intake by increasing glucose storage and utilization. 4. Autonomic Responses: ○ The LH sends projections to the spinal cord, controlling autonomic processes such as digestive secretions, which aid in food digestion and nutrient absorption. Impact of Damage or Stimulation:  Damage: ○ Lesions in the LH lead to a refusal to eat or drink, often requiring force-feeding to sustain life. This is associated with a diminished taste response and impaired digestion. ○ Such damage also disrupts dopamine pathways passing through the LH, impairing reward and motivation related to eating. Stimulation: ○ Activation of the LH increases the drive to eat, overriding satiety signals. The Ventromedial Hypothalamus (VMH) The VMH serves as an inhibitor of feeding, opposing the actions of the LH. It integrates signals about satiety and energy homeostasis and influences metabolic processes. Functions of the Ventromedial Hypothalamus: 1. Inhibition of Feeding: ○ The VMH regulates feeding suppression by responding to signals such as leptin (produced by fat cells) and other satiety-related hormones. 2. Metabolic Regulation: ○ Damage to the VMH disrupts metabolic balance, causing increased insulin secretion, which accelerates fat storage and leads to persistent hunger. 3. Behavioral and Digestive Impact: ○ Damage to the VMH increases the frequency of meals due to rapid gastric emptying and heightened gastrointestinal motility. Impact of Damage or Stimulation: Damage: ○ Lesions in the VMH lead to overeating and dramatic weight gain (ventromedial hypothalamic syndrome). ○ While meal sizes remain normal, the frequency of meals increases due to heightened insulin production and fat storage, leaving blood glucose levels low and cells "starved." ○ These effects extend beyond the nucleus to involve surrounding regions for more pronounced symptoms. Stimulation: ○ Activation of the VMH suppresses feeding behavior and slows metabolic processes. Key Insights: The LH operates as a feeding facilitator by coordinating sensory, motor, and autonomic processes, ensuring food intake is efficient and rewarding. When disrupted, it can cause profound reductions in feeding behaviors. The VMH acts as a brake on feeding, regulating meal frequency and the storage of energy. Disruptions in its functioning lead to metabolic imbalances, excessive fat accumulation, and constant hunger. Eating Disorders Overview 1. Homeostatic Control and Its Failures: ○ Insulin, leptin, glucose, and other factors regulate hunger but are not foolproof. ○ Obesity results partly from evolutionary predispositions to eat during food abundance. ○ Anorexia and bulimia illustrate complex dysfunctions in feeding behavior. Obesity 1. Psychological Factors: ○ Weak correlation between mood and long-term weight gain. ○ Obesity is only modestly linked to depression. 2. Prenatal Influences: ○ High-fat maternal diets may permanently alter offspring's appetite-regulating brain regions. 3. Genetic Influences: ○ Syndromal Obesity: Genes like ghrelin dysregulation in Prader-Willi syndrome. ○ Monogenic Obesity: Mutations in single genes (e.g., melanocortin receptor). ○ Polygenic Obesity: Interaction of multiple genes with small effects, such as FTO variants. 4. Environmental Interaction: ○ Lifestyle and diet significantly amplify genetic predispositions, as seen in Pima populations. 5. Weight Loss Techniques: ○ Gradual dietary changes, consistent moderate exercise, and avoiding sugary drinks are effective. ○ Surgical and pharmacological interventions exist but have limitations and risks. ○ Experimental approaches (e.g., gut microbiome manipulation) show promise. Bulimia Nervosa 1. Characteristics: ○ Cycles of binge eating and purging/dieting. ○ Biochemical changes like elevated ghrelin appear as a result rather than a cause. 2. Addiction-Like Behavior: ○ Similarities between bulimia and substance addiction include dopamine and opioid activity. ○ Animal studies suggest parallels in withdrawal symptoms. Anorexia Nervosa 1. Characteristics: ○ Fear of gaining weight, preference for low-calorie foods, and excessive physical activity. ○ Affects about 1% of women and 0.33% of men, often beginning in adolescence. 2. Potential Causes: ○ Weight loss may drive psychological and biochemical abnormalities rather than depression or other pre-existing factors. 3. Animal Model Insights: ○ Rats on extreme caloric restriction and exposed to cold exhibit anorexia-like behaviors. 4. Innovative Treatment: ○ Strategies include keeping patients warm, limiting physical activity, and guided food intake using technology. ○ Promising results in Europe suggest this approach may outpace traditional methods. The brain areas that control eating monitor taste, blood glucose, stomach distension, duodenal contents, body weight, fat cells, hormones, social influences, and more. Because the system is so complex, it can produce errors in many ways. However, the complexity of the system also provides a kind of security: If one part of the system makes a mistake, another part can counteract it. We notice people who choose a poor diet or eat the wrong amount, but perhaps we should be even more impressed by how many people eat appropriately. The regulation of eating succeeds not in spite of its complexity but because of it.