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This document contains Chapters 9 to 10 Chapter 9 Energy Metabolism Overview In Chapter 9, students will learn how the body derives energy from energy-yielding nutrients. Adenosine triphosphate is defined as the energy currency used by cells. The chemistry of oxidation-reduction reactions is reviewed to lay the groundwork for the metabolic pathways of carbohydrate, fatty acid, protein, and alcohol metabolism discussed throughout the chapter. The interrelationships among the various metabolic pathways is emphasized, with intermediates from one pathway participating in other pathways to ensure that all body cells have energy for survival, even in times of fasting and semistarvation. The regulation of metabolism by the liver, cellular energy levels, hormones, enzymes, vitamins, and minerals is presented. The chapter concludes with several examples of inborn errors of metabolism, in which a genetic defect at any point within a metabolic pathway can cause illness or death.
Learning Outcomes Characterize the properties of metabolism, catabolism, and anabolism. Describe oxidation and reduction reactions. Illustrate the metabolic pathways involved in ATP production from carbohydrates. Illustrate the metabolic pathways involved in ATP production from fats. Discuss how ATP production from protein differs from catabolism of carbohydrate and fat. Illustrate the process of gluconeogenesis. Discuss how the body metabolizes alcohol. Summarize how fed and fasted states affect metabolism. Describe common inborn errors of metabolism. Teaching Strategies, Activities, Demonstrations, and Assignments Assign students the Take Action activity, “Weight Loss and Metabolism.” Assign students the Take Action activity at the end of the chapter, “Newborn Screening in Your State.” Have students write a memo in class to another classmate explaining one of the metabolic pathways or an aspect of the pathway(s) that is unclear. Have the student respond to their classmate’s concern. Collecting these memos will help you to gauge where your students are in understanding the pathways. Use the Case Study of a woman considering a very-low carbohydrate diet to lead a discussion of low-carbohydrate, high-protein diets and their potential effects on the body. Ask students to look up ketones in low-carbohydrate diet books and compare that information with the information have learned in class. Discuss the impact of ketone production on body organs and possible health risks. Using pathway illustrations from the text create cardboard labels and hand them out to students. Draw the pathway arrows on the board and have students place their label in the appropriate location. Have the students compare and contrast the adaptations that occur during the fasting state and the feasting state. What does fasting encourage? What does feasting encourage? Lecture Outline Metabolism: Chemical Reactions in the Body General Metabolism: entire network of chemical processes involved in maintaining life Release of energy from macronutrients and alcohol Synthesis of new substances Prepare wastes for excretion Metabolic pathway: group of biochemical reactions that occur in sequence Anabolic: use small, simple compounds to build large, complex compounds; growth Catabolic: break down compounds into smaller units; weight loss or wasting In general, balance exists between anabolism and catabolism Intermediates: compounds formed within a metabolic pathway Converting Food into Energy Sources: catabolic reactions that break chemical bonds in monosaccharides, fatty acids, amino acids, glycerol, and alcohol (originally produced during photosynthesis) to form ATP, heat, carbon dioxide, and water Adenosine Triphosphate (ATP) Main form of energy used by body Structure: adenosine bound to 3 phosphate groups The bonds between the phosphate groups contain energy To release energy from ATP, hydrolysis of one phosphate yields adenosine diphosphate (ADP) plus a free phosphate group, then adenosine monophosphate (AMP) + Pi ATP is constantly recycled within cells Body contains 0.22 lbs. (100 g) of ATP Sedentary adult uses 88 lbs. (40 kg) of ATP/day During 1 hour of strenuous exercise, 66 lbs. (30 kg) of ATP are used Oxidation-Reduction Reactions: Key Processes in Energy Metabolism Oxidation-reduction reactions transfer electrons, mainly hydrogen ions, from energy-yielding compounds to oxygen, forming water and energy for ATP synthesis from ADP + Pi Oxidation and reduction occur together Inorganic substance is oxidized: loss of 1 or more electrons (LEO) Inorganic substance is reduced: gain of 1 or more electrons (GER) Organic substance is oxidized: gain of oxygen or loss of hydrogen; hydrogen atoms are eventually added to oxygen to form water Organic substance is reduced: loss of oxygen or gain of hydrogen Oxidation-reduction reactions are controlled by enzymes (e.g., dehydrogenases) Niacin and Riboflavin: Key Players in Energy Metabolism Nicotinamide adenine dinucleotide (contains niacin) Oxidized form: NAD+ Reduced form: NADH Flavin adenine dinucleotide (contains riboflavin) Oxidized form: FAD Reduced form: FADH2 ATP Production from Carbohydrates General ATP is generated through cellular respiration: oxidation of food molecules to obtain energy; oxygen is final electron acceptor Aerobic: oxygen is readily available; cellular respiration is more efficient (net gain of 30 - 32 ATP from glucose) Anaerobic: oxygen is not present; cellular respiration is less efficient (net gain of 2 ATP from glucose) Glycolysis (see Figure 9-7 and Appendix C) Break down carbohydrates to generate energy: 1 glucose (6 carbons) is oxidized to form 2 pyruvate (3 carbons), NADH + H+, and net of 2 ATP Glucose activated by conversion to glucose 6-phosphate; requires ATP Glucose 6-phosphate converted to fructose 6-phosphate Fructose 6-phosphate converted to fructose 1,6-bisphosphate, requires ATP Fructose 1,6-bisphosphate splits into glyceraldehyde 3-phosphate and dihydroxyacetone 3-phosphate; dihydroxyacetone 3-phosphate is converted to glyceraldehyde 3-phosphate, so following steps occur twice per glucose molecule Glyceraldehyde 3-phosphate converted to 1,3-bisphosphoglycerate to produce NADH + H+ 1,3-bisphosphoglycerate converted to 3-phosphoglycerate, transferring phosphate to ADP to generate ATP Water is removed from 3-phosphoglycerate to generate phosphoenolpyruvate Phosphate transferred from phosphoenolpyruvate to ADP to generate ATP and pyruvate Provide building blocks for synthesis of other compounds Occurs in cytosol Transition Reaction: Synthesis of Acetyl-CoA (see Figure 9-6) Pyruvate is oxidized and joined with CoA to form acetyl-CoA, NADH + H+, and CO2 Catalyzed by pyruvate dehydrogenase Irreversible transition reaction Occurs in mitochondria Requires four B-vitamins Thiamin Riboflavin: FADH or FADH2 Niacin: NAD+ or NADH Pantothenic acid: precursor to CoA Citric Acid Cycle (see Figure 9-8 and Appendix C) Alternate names for citric acid cycle Tricarboxylic acid (TCA) cycle Krebs cycle Acetyl-CoA leads to production of NADH + H+, FADH2, ATP, and CO2 Acetyl CoA (2 carbons) combines with oxaloacetate (4 carbons) to form citrate (6 carbons), releasing CoA Citrate (6 carbons) is oxidized to form alpha-ketoglutarate (5 carbons), NADH + H+, and CO2 Alpha-ketoglutarate (5 carbons) is oxidized to form succinate (4 carbons), NADH + H+, and CO2 Succinate (4 carbons) is oxidized to form fumarate (4 carbons) and FADH2 With the input of water, fumarate (4 carbons) is oxidized to form oxaloacetate (4 carbons) and NADH +H+ Occurs in mitochondria Does not require oxygen Two cycles per glucose molecule Each cycle yields 2 CO2 1 GTP (potential for ATP) 3 NADH + H+ 1 FADH2 Electron Transport Chain (see Figure 9-9 and Appendix C) NADH + H+ are oxidized to NAD+, and FADH2 is oxidized to FAD to produce ATP and water Occurs in mitochondria Produces 90% of ATP from glucose As electrons are passed from one carrier to the next, small amounts of energy are released (oxidative phosphorylation) NADH + H+ and FADH2 transfer hydrogen and electrons to electron carriers on inner mitochondrial membrane Hydrogen ions are pumped into the compartment between the inner and outer mitochondrial membrane NAD+ and FAD are available to function in glycolysis, the transition reaction, and the citric acid cycle Coenzyme Q separates pairs of electrons and passes them onto cytochromes; energy is released by each transfer Some energy used to pump H+ into the outer mitochondrial compartment Some energy is used to generate ATP from ADP + Pi Much energy is released as heat H+ diffuse into inner mitochondrial compartment through special channels, ATP synthase produces ATP from ADP + Pi At the end of the electron transport chain, electrons, H+ and oxygen combine to form water ATP is transported out of inner mitochondrial compartment by a carrier that exchanges ATP for ADP Requires minerals Copper: component of enzyme Iron: component of cytochromes (electron-transfer compound) The Importance of Oxygen NADH + H+ and FADH2 from citric acid cycle are regenerated to NAD+ and FAD by transfer of their electrons and hydrogen to oxygen in the electron transport chain Without oxygen, cells would not be able to generate sufficient energy to sustain life Anaerobic Metabolism For cells that are not capable of aerobic respiration (lack mitochondria; e.g., RBCs) or need to produce energy in the absence of oxygen (e.g., during intense exercise), pyruvate may be converted to lactate, providing only 5% of potential ATP Transfer of hydrogen from NADH + H+ to pyruvate produces lactate + NAD+ NAD+ continues function of glycolysis Lactate is released into bloodstream, picked up by liver, and used to synthesize pyruvate, glucose, or some other intermediate in aerobic respiration Cori Cycle (see Figure 9-10) During high intensity exercise muscle cells rely on anaerobic glycolysis to quickly produce ATP Causes lactate accumulations and NAD+ regeneration Regenerated lactate is transported back to liver from muscles and converted to glucose and returned to muscle Overall energy yield of aerobic respiration Each NADH yields 2.5 ATP Each FADH2 yields 1.5 ATP Each GTP yields 1.0 ATP Total ATP from each glucose molecule = 32 ATP Glycolysis  2 ATP Citric acid cycle (GTP)  2 ATP Electron transport chain (ATP)  28 ATP ATP Production from Fats General Lipolysis: breakdown of triglycerides into free fatty acids and glycerol Fatty acid oxidation: breakdown of fatty acids for energy production; net donation of electrons from fatty acids to oxygen; takes place in mitochondria Sources of fatty acids for oxidation Dietary fat (e.g., following high-fat meal) Fat stored in adipose tissue (e.g., in fasting state) Release of fat from adipose cells relies on hormone-sensitive lipase Hormone-sensitive lipase activity is affected by: Glucagon (increases HSL activity) Growth hormone (increases HSL activity) Epinephrine (increases HSL activity) Insulin (decreases HSL activity) Fatty acids are shuttled from cytosol into mitochondria by carnitine ATP Production from Fatty Acids Most fatty acids in nature have even number of carbons (2 to 26) Beta-oxidation: 2-carbon fragments from a fatty acid are cleaved and converted to acetyl-CoA (see Figure 9-13) Begins with beta carbon: second carbon at the carboxyl end Produces NADH + H+ and FADH2 Acetyl-CoA enters citric acid cycle to produce CO2 and ATP Glucose yields 5 ATPs/carbon 16-carbon fatty acid yields 7 ATPs/carbon, due to fewer oxygen atoms than glucose Carbohydrate Aids Fat Metabolism Some intermediates of citric acid cycle enter other biosynthetic pathways, which depletes oxaloacetate supply Formation of pyruvate from carbohydrate metabolism replenishes oxaloacetate Ketones: By-products of Fat Catabolism Ketone bodies: products of incomplete fatty acid oxidation, mostly resulting from hormonal imbalances (e.g., inadequate insulin production) Acetoacetic acid Beta hydroxybutyric acid Acetone Ketosis: excess of ketone bodies (see Figure 9-15) Build-up of acetyl CoA; join together to form ketone bodies Characterized by fruity breath odor (from excretion of acetone via lungs) Most ketone bodies are converted back into acetyl-CoA and metabolized via citric acid cycle Ketosis in Diabetes Lack of insulin inhibits normal carbohydrate and fat metabolism Cells cannot utilize glucose, so fatty acids are rapidly metabolized to ketone bodies Excessive ketones are excreted in urine along with sodium and potassium, leading to ion imbalances Diabetic ketoacidosis (typically only seen with uncontrolled type 1 diabetes) pH of blood decreases May lead to coma or death Treatment: insulin, electrolytes, fluids Ketosis in Semistarvation or Fasting Low insulin production during semistarvation or fasting causes fatty acids to flood the bloodstream and form ketone bodies in the liver Ketone bodies may be used for fuel by heart, muscles, kidneys, and brain (after several days) As cells adapt to using ketones for fuel, less glucose is produced from amino acids (sparing protein) Death occurs after 50 - 70 days of total fasting, when about half of body protein is depleted Protein Metabolism General Metabolism of protein takes place primarily in the liver Muscle metabolism of protein is limited to branched-chain amino acids (leucine, isoleucine, and valine) Deamination: removal of amino group from amino acid; often requires vitamin B-6 Produces carbon skeletons that serve as intermediates in citric acid cycle or yield acetyl-CoA or pyruvate Glucogenic amino acids Amino acids that can be used to form pyruvate Alanine Glycine Cysteine Serine Threonine Amino acids that can enter the citric acid cycle directly Asparagine Arginine Aspartic acid Histidine Glutamic acid Glutamine Isoleucine Methionine Proline Valine Phenylalanine Ketogenic amino acids that become acetyl-CoA (cannot become part of glucose molecules) Leucine Lysine Part of isoleucine Part of phenylalanine Part of tryptophan Part of tyrosine Gluconeogenesis: Producing Glucose from Glucogenic Amino Acids and Other Compounds Gluconeogenesis: generation of glucose from certain amino acids in liver and some kidney cells In the mitochondria, carbon skeleton of a glucogenic amino acid is converted to oxaloacetate Oxaloacetate moves to cytosol, loses 1 CO2, becomes phosphoenolpyruvate Phosphoenolpyruvate reverses the path through glycolysis to glucose Gluconeogenesis requires ATP, biotin, riboflavin, niacin, and vitamin B-6 Gluconeogenesis from Typical Fatty Acids Is Not Possible Fatty acids with even number of carbons are broken down to acetyl-CoA The reaction that converts pyruvate to acetyl-CoA is irreversible Acetyl-CoA may only form ketones and/or combine with oxaloacetate in the citric acid cycle During citric acid cycle, acetyl-CoA is added to oxaloacetate, but 2 carbons are lost as CO2; thus, no carbons from acetyl-CoA remain to form glucose Glycerol portion of triglyceride may be converted to glyceraldehyde 3-phosphate to yield glucose; yield is insignificant Disposal of Excess Amino Groups from Amino Acid Metabolism Amino groups (-NH2) are converted to ammonia (NH3),which is toxic to cells In the liver, ammonia is converted to urea by the urea cycle 2 nitrogen groups (1 NH2 and 1 NH3) react with CO2 to form urea and water Urea is excreted via urine Nitrogen in blood is a sign of organ disease High [NH3] = liver disease High [urea] = kidney disease Global Perspective: Cancer Cell Metabolism Cancer is characterized by abnormal, unregulated cell growth Disrupting metabolism of cancer cells is an area of investigation for potential cancer treatment In cancer cells, even when oxygen is plentiful, cancer cells use glycolysis and produce lactate, known as the Warburg effect As cancer cells use up glucose, they starve healthy cells of energy and nutrients; cells weaken and die, giving cancer cells space to proliferate Excessive nutrient use by cancer cells produces free radicals, which may increase DNA mutations and promote cancer Cancer cells also use protein and fat wastefully Cancer cells use glutamine at a high rate, which impairs normal protein synthesis in the body Cancer cells use fat mostly to make lipids and phospholipids needed for their cell membranes Cancer cells die when glucose is withdrawn Potential treatments involve blocking the enzymes during metabolism Alcohol Metabolism (see Figure 9-19) Alcohol dehydrogenase (ADH) pathway is main way alcohol is metabolized Alcohol  acetaldehyde by alcohol dehydrogenase; yields NADH + H+ Acetealdehyde  acetyl-CoA by aldehyde dehydrogenase; yields NADH + H+ Occurs mainly in liver, although 10 - 30% may occur in stomach lining cells Fate of acetyl-CoA Some may enter citric acid cycle, but ADH pathway limits supply of NAD+; ADH pathway takes priority over citric acid cycle in cells Most is directed to fatty acid and triglyceride synthesis Results in steatosis: accumulation of fat in the liver Characterized by high blood triglycerides Microsomal ethanol oxidizing system (MEOS) metabolizes alcohol intake in excess of capacity of ADH pathway Uses oxygen and NADP to produce water and acetaldehyde Uses potential energy (NADPH + H+) rather than yielding potential energy (NADH + H+ in ADH pathway) Catalase pathway is minor Exceeding capacity of alcohol metabolizing systems leads to alcohol poisoning Regulation of Energy Metabolism Overview of metabolic pathways Glycolysis (glucose  pyruvate) in cytosol Transition reaction (pyruvate  acetyl-CoA) in mitochondria Citric acid cycle (acetyl-CoA  CO2) in mitochondria Gluconeogenesis in mitochondria and cytosol Beta oxidation (fatty acid  acetyl CoA) in mitochondria Glucogenic amino acid oxidation (amino acids  pyruvate) in cytosol Non-glucogenic amino acid oxidation (amino acids  acetyl-CoA) in mitochondria Alcohol oxidation (ethanol  acetaldehyde) in cytosol Alcohol oxidation (acetaldehyde  acetyl-CoA) in mitochondria The Liver (see Figure 9-21) Conversions between various simple sugars Fat synthesis Production of ketone bodies Amino acid metabolism Urea production Alcohol metabolism Nutrient storage ATP Concentrations High [ATP] decreases energy-yielding reactions and increases anabolic reactions High [ADP] increases energy-yielding pathways Enzymes, Hormones, Vitamins, and Minerals Enzymes Presence (i.e., enzyme synthesis) Rate of activity Hormones Regulate metabolic processes Low [insulin] promotes gluconeogenesis, protein breakdown, and lipolysis High [insulin] promotes synthesis of glycogen, fat, and protein Vitamins and minerals (see Figure 9-22) Thiamin Riboflavin Niacin Pantothenic acid Biotin Vitamin B-6 Folate Vitamin B-12 Iron Copper Vitamin C Vitamin K Magnesium Fasting and Feasting Fasting Postprandial fasting (0 - 6 hours after eating) Use of carbohydrate (glycogen from the liver) Use of fat (from adipose stores) Use of protein (from body fat) Short-term fasting (3 - 5 days) Use of carbohydrate (glycogen stores are exhausted) Fatty acid oxidation continues Gluconeogenesis (amino acids from lean tissue and glycerol from triglycerides  glucose) to provide fuel for CNS and RBCs Early gluconeogenesis leads to rapid breakdown of lean tissue (supplies 90% of glucose) that would lead to death within 2- 3 weeks Sodium and potassium are also depleted via urine when ketone bodies are excreted Blood urea levels increase Long-term fasting (5+ days) Metabolic rate slows, reduces energy requirements CNS begins to use ketone bodies When lean body mass declines by 50% (7 - 10 weeks), death occurs Feasting Accumulation of body fat Insulin production encourages use of glucose for energy, synthesis of glycogen, and storage of protein and fat Fat consumed in excess of need is stored in adipose cells (requires little energy) Protein consumed in excess of need does not promote muscle development Some remains in blood’s amino acid pool (minor) Some used to synthesize fatty acids (minor; costly process requires ATP, biotin, niacin, and pantothenic acid) Some metabolized for energy Carbohydrate consumed in excess of need Maximize glycogen stores Used as fuel, lessens need for fat catabolism Storage as fat (not an active pathway in humans; uses ATP, biotin, niacin, and pantothenic acid) Synthesis of fat from carbohydrate or protein (lipogenesis) takes place in cytosol of liver cells Acetyl-CoA from glucose or amino acids is linked into palmitic acid (16-carbon fatty acid) Insulin increases activity of fatty acid synthase, which regulates lipogenesis Palmitic acid can be lengthened to 18- or 20-carbon chain Used to synthesize triglycerides Clinical Perspective: Inborn Errors of Metabolism General Lack of enzyme to perform a specific metabolic function Products of disrupted metabolism may be toxic to the body Inherit defective gene from one or both parents (may not have the disease, but are carriers) Symptoms of disorder appear shortly after birth (e.g., loss of appetite, vomiting, dehydration, weakness, developmental delays) Specific - involve 1 or a few enzymes No cure, only treatment Newborn Screening Public health program that provides early identification and follow-up treatment of infants with genetic and metabolic disorders Components of screening are state-specific Phenylketonuria (PKU) 1/13,500 -19,000 births Most common among people of Irish descent Carriers are detected by simple blood test Newborn screening for PKU is required in all states Inefficient function of phenylalanine hydroxylase in liver Normal metabolism: phenylalanine  tyrosine PKU leads to accumulation of phenylalanine and byproducts to toxic levels, which leads to mental retardation Deficiency of tyrosine Treatment Phenylalanine-restricted diet (phenylalanine cannot be omitted because it is an essential amino acid) Continual monitoring of infants through blood testing Specialized infant formulas are needed to meet high protein needs without high phenylalanine Foods with low phenylalanine content (fruits, vegetables) Foods with moderate phenylalanine content (breads, cereals) Foods with high phenylalanine content (dairy products, eggs, meats, nuts, cheeses, aspartame) Older children and adults must still rely on low-phenylalanine formula Low-phenylalanine diet must be continued throughout life or decreased intelligence and behavioral problems occur During pregnancy, exposure to toxic levels of phenylalanine may lead to miscarriage or birth defects Galactosemia 1/47,000 births Most common among people of Italian and Irish descent 2 specific enzyme defects lead to reduced metabolism of galactose to glucose; buildup of galactose can lead to serious bacterial infections, mental retardation, and cataracts Infants with galactosemia develop vomiting after a few days of infant formula or breast milk Treatment Soy formula Avoidance of certain foods (lactose-containing products, organ meats, some fruits and vegetables) Strict label reading Glycogen Storage Disease 1/60,000 births Inability to convert glycogen to glucose due to one of a number of enzyme defects Symptoms Poor growth Low blood glucose Liver enlargement Treatment Frequent meals to regulate blood glucose Raw cornstarch (slowly digested, maintains blood glucose) Careful monitoring of blood glucose Chapter 10 Energy Balance, Weight Control, and Eating Disorders Overview Chapter 10 begins with a discussion of energy balance and the components of energy expenditure - basal metabolic rate, physical activity, thermic effect of food, and thermogenesis. Various methods for measuring energy expenditure, including direct and indirect calorimetry, are presented. Next, students will learn about the differences between hunger and appetite as well as the many factors that influence appetite. Methods for estimating body composition are reviewed, including BMI, underwater weighing, air displacement, DEXA, and skinfold thickness. Sensible weight-loss treatments are compared to fad diets. Medical interventions for weight control, such as very-low-calorie diets, weight-loss medications, and gastroplasty are reviewed. The chapter concludes with a discussion of the diagnosis, characteristics, treatment, and prevention of eating disorders, including anorexia nervosa, bulimia nervosa, and binge-eating disorder. Learning Outcomes Describe energy balance and uses of energy by the body. Compare methods used to measure energy expenditure by the body. Explain internal and external regulation of hunger, appetite, and satiety. Discuss methods for assessing body composition and determining whether body weight and composition are healthy. Describe the impact of genetics and environment on body weight and composition. Outline the key components of programs designed to treat overweight, obesity, and underweight. Discuss the characteristics of fad diets. Evaluate weight-loss programs to determine whether they are safe and likely to result in long-term weight loss. Describe eating disorders and methods for reducing their development. Teaching Strategies, Activities, Demonstrations, and Assignments 1. Assign students the Take Action activity, "Changing for the Better." They should complete the calculations and the interpretation and application sections. They should turn this assignment in to be graded. 2. Have students read a popular diet book or current magazine article describing a weight-loss plan. They can use Table 10-7 as a guide for making their choice. Have them read the book and do the following: A. Write a report evaluating the book/article, using the principles of a sound weight-loss program and characteristics of fad diets listed in the chapter as guides. Have them address weaknesses and strengths of the diet approach, faddist tendencies, and violations of sound weight-loss principles. B. Evaluate the diet described by the book, using the Dietary Guidelines for Americans 2010 for comparison. C. These reports could be used as a basis for making oral reports on various diets. 3. Have students revise their own dietary record that they kept to do their nutritional assessment earlier in the semester to make it nutritionally adequate and to provide 1,200 kcal/d/women and 1,500 kcal/d/men. Some will need to add and others eliminate or decrease foods to reach these kilocalories. Have them use the Dietary Guidelines for Americans 2010 to determine nutritional adequacy of the diet they have created. 4. Have students select three food products for which claims are made like "low calories," "light," "reduced calories," or "dietetic," and compare that product to a similar one for which no claim is made for energy and nutrient content. For example, comparing reduced-calorie mayonnaise to regular. 5. Have students bring an advertisement for a weight-reduction aid to class. Select from these and have the class evaluate, in writing or as a class discussion, the rationale, effectiveness, cost, and potential hazards. 6. Have students get menus from area restaurants and fast-food establishments. Put these menus on an overhead transparency. Use the overheads for class discussion. Ask students to choose foods and meals from these menus that would be appropriate for weight control. 7. Use a class period to allow students to go to a campus facility to have their body fat assessed using skinfold thicknesses. If there are no campus resources, ask someone from a local fitness center to do it, or do it yourself with the help of another faculty member of the opposite gender (so the female and male could assess same-gender students). Most exercise physiology books have formulas and instructions for doing skinfold measurements. 8. Ask a resource from the community to lecture in your class about various weight control issues: A. Ask a physician to discuss treatment for morbid obesity. B. Ask leaders from TOPS or Weight Watchers to discuss their approaches and programs. 9. Divide students into groups. Have each group compile three lists. The first list should contain healthful eating tips; for example, trim fat from meat before cooking. The second list should contain helpful dieting tips, for example, cut vegetables, dried fruit, and pretzels are good snack choices when traveling in a car. The third list should contain dieting traps and ways to prevent being "trapped." An example would be the restaurant ordering trap. The prevention tip would be to think of what would be healthful food choices before entering the restaurant. And, once in the restaurant, be the first to order if you are with others so their choices will not influence yours. Use the lists as a springboard for discussing behavior modification. Collect the lists, consolidate information, have someone type resulting lists, and either photocopy for students or make a copy available for interested students to photocopy. 10. Ask students to wear pedometers for five days to track the number of miles they walk. Have them calculate the number of calories burned based on the distance walked. (Students can use their diet analysis software if you prefer.) 11. Ask a professional from your community who treats eating disorders to give a guest presentation in the class. It might be preferable to have someone from the campus counseling center do this presentation so students can become familiar with a campus resource for treating eating disorders. 12. Ask an individual who is recovering from an eating disorder to give a presentation in class about his or her history and condition, and give opportunities for students to ask questions. Ask the guest speaker to discuss how he/she developed the disorder, triggers or cues to binging, his/her life characteristics, and what prompted him/her to get treatment. 13. Have students investigate resources in the university or the community for individual and/or group services to help students with eating disorders. 14. Prepare a "case study" description of anorexia nervosa or bulimia (or use one of the available films) and have students analyze the "case" to identify: A. Initiation or triggering factors B. Signs and symptoms C. Presence of "typical" characteristics D. Warning signs E. Prognosis with treatment 15. Have students bring to class examples from the media related to body image. Discuss what the media is telling us about our bodies/images. What influence do these messages have on an individual who is at risk to develop an eating disorder?
Lecture Outline Energy Balance General Energy balance: relationship between energy intake and energy expenditure Energy equilibrium: calories consumed = energy expended Positive energy balance: calories consumed > energy expended, leads to growth, weight gain, recovery from illness or injury Weight gain is not a natural part of aging; it stems from a pattern of excess food intake coupled with limited physical activity and slower metabolism Negative energy balance: calories consumed carbohydrate > fat Large meal > many small meals Adaptive Thermogenesis Heat produced when body expends energy for non-voluntary physical activity (e.g., shivering, fidgeting, maintaining muscle tone) Also known as Thermoregulation Non-exercise activity thermogenesis (NEAT) Brown adipose tissue: specialized fat tissue that participates in thermogenesis High amount of uncoupling protein Mostly found in infants (as much as 5% of body weight) and hibernating animals Measuring Energy Expenditure Direct calorimetry Measures amount of heat released by a person in an insulated chamber surrounded by a layer of water Expensive and complex equipment Indirect calorimetry Based on predictable relationship between energy use and O2 consumption and CO2 production, as measured in expired air Measured in laboratory or with a handheld device (mobile) Doubly labeled water Subject consumes doubly labeled water (2H2O and H218O) Blood and urine samples are analyzed to examine excretion of 2H (excreted only as water) and 18O (excreted as CO2 in expired air) Compare hydrogen losses to oxygen losses to measure carbon dioxide output Accurate, but expensive Estimated Energy Requirements (EERs) developed by Food and Nutrition Board to estimate energy needs based on weight (kg), height (m), gender, age (years), and physical activity level (see tables) Adult men: EER = 662 - (9.53 x AGE) + PA x ([15.91 x WT] + [539.6 x HT]) Adult women: EER = 354 - (6.91 x AGE) + PA x [(9.36 x WT[ + [726 x HT[) Eating Behavior Regulation Hunger: physiological drive to find and eat food controlled by internal body mechanisms (e.g., organs, hormones, hormone-like factors, nervous system) Appetite: psychological drive to eat affected mostly by external factors (e.g., social customs, time of day, mood, tastes, sight) External signals cause cephalic responses by the body: release of saliva, digestive hormones, and insulin that encourage eating and prepare the body for the meal Although hunger and appetite work together, they don’t always coincide; where food is ample, appetite is the main trigger for eating Satiety: satisfaction after eating; cessation in drive to eat Regulated by hypothalamus, which communicates with the endocrine and nervous systems and integrates internal cues (e.g., blood glucose levels, hormone secretions, and sympathetic nervous system activity) Damage to satiety center (e.g., from cancer or surgery) may lead to obesity or weight loss Satiety process Sensory aspects of food Knowledge that a meal has been eaten Release of histamine in response to chewing Gastrointestinal distension Secretion of hormones (e.g., cholecystokinin, glucagon-like peptide-1, and peptide YY3-36) during digestion Nutrient receptors in the small intestine Apolipoprotein on chylomicrons Metabolism of nutrients Carbohydrates increase serotonin production Protein decreases secretion of ghrelin Nutrient use in the liver Body fat: adipose cells secrete leptin, which signal satiety, although leptin seems more important for promoting energy conservation Signals to eat Fall in macronutrient concentrations in blood Release of endorphins Hormones (e.g., ghrelin) Estimating Body Weight and Composition Weight-for-Height tables Metropolitan Life Insurance Company tables (latest in 1983) considered gender and frame size Better for estimating health and longevity of populations than for determining individual health status Recent shift of focus from weight to body fat, location of body fat, and weight-related medical problems Body Mass Index Current standard Most closely related to body fat content Kg/m2 or (lb x 703)/in2 BMI categories Underweight: 30 or BMI > 27 with comorbid conditions and no contraindications Examples Medications that enhance norepinephrine and serotonin activity in the brain by reducing reuptake by nerve cells; prolongs sense of satiety Amphetamine-like medications that prolong epinephrine and norepinephrine activity in the brain; show only short-term effectiveness (e.g., phenteramine) Medications that inhibit lipase enzyme action in the small intestine, reducing fat digestion by about 30% (e.g., orlistat); requires control of fat intake and use of multivitamin and mineral supplement to compensate for nutrient losses in feces Off-label use of medications that have weight loss as a side effect (e.g., antidepressants, such as bupropion) Treatment of Severe Obesity Severe (morbid) obesity: at least 100 lb over (or 2X) healthy body weight Very-low-calorie diets (VLCDs) or modified fasts (e.g., Optifast) Provide 400 - 800 kcal/d, often in liquid form Most often used by those with poorly-controlled, obesity-related diseases Usually induce ketosis, which decreases hunger Main reasons for weight loss are calorie restriction and absence of food choices Loss of 3- 4 lb/week Careful monitoring by physician is crucial to avoid heart problems and gallstones Maintenance is difficult, depends on behavioral changes and physical activity Gastroplasty (see Figure 10-18) Candidates are morbidly obese, have been obese > 5 years, previous attempts at non-surgical weight loss, no history of alcoholism or major psychiatric disorders Gastric bypass surgery: reduces stomach capacity to 30 ml, bypasses part of upper small intestine to promote malabsorption of nutrients Vertical-banded gastroplasty: staples stomach to create a small pouch; bands stomach outlet Gastric banding: band placed around upper portion of stomach to create small pouch; adjust band by injecting with saline solution Requires major lifestyle changes Frequent, small meals Elimination of sugars to prevent dumping syndrome (severe diarrhea that occurs with consuming concentrated sources of sugar) Costly 75% of those undergoing gastroplasty lose half or more of excess body weight; long-term maintenance leads to dramatic health improvements (e.g., reduced blood pressure and elimination of type 2 diabetes) Risks (bleeding, blood clots, hernias, infections, 2% death date, nutrient deficiencies) May require future surgery to remove excess skin Treatment of Underweight BMI < 18.5 Health risks of underweight Loss of menstrual function Low bone mass Complications with pregnancy and surgery Slow recovery after illness Stunted growth and development Increased death rates, especially combined with cigarette smoking Causes Excessive physical activity Severe calorie restriction Health conditions (e.g., cancer, infectious disease, digestive tract disorders, mental stress or depression) Genetic background Weight gain requires 500 extra kcal/d Replace low-energy-density foods with high-energy- density foods Gradually increase portion sizes Eat regular meals Reduce excessive physical activity Build lean mass through resistance training Eating Disorders General Disordered eating: mild and short-term changes in eating patterns that occur in response to a stressful event, illness, or desire to modify the diet for health and/or appearance Eating disorder: severe distortion of the eating process that can develop into a life-threatening condition if left untreated Prevalence and Susceptibility Statistics Affect more than 5 million people in North America 6 to 10 times more common in females than males Most likely to develop during adolescence or early adulthood Up to 5% of women in North America develop some form of anorexia nervosa or bulimia nervosa during their lifetimes Genetics Psychology Physiology Eating disorders may start with simple diet, but because of stress, lack of appropriate coping mechanisms, dysfunctional family relationships, or drug abuse, dieting gets out of control Frequently coincide with psychological disorders (e.g., depression, substance abuse, anxiety disorders) Eating disorders require professional intervention that goes beyond nutritional therapy Anorexia Nervosa General Denial of appetite; disgust with one’s body Extreme weight loss Distorted body image Fear of obesity and weight gain ~1 in 200 adolescent girls in North America eventually develops AN Associated with weight gain that occurs naturally during puberty Only 10% of cases occur in men, and those are usually related to participation in sports that require weight classes Typical characteristics of those with eating disorders (see Table 10-8) Rigid dieting, causing weight loss to less than 85% of normal weight False body perception Maintenance of rigid control in lifestyle Feeling of panic after small weight gain Feeling of purity, power, or superiority through maintenance of strict discipline Preoccupation with food Helplessness in presence of food Lack of menstrual period Possible presence of binging and purging practices Physical Effects of Anorexia Nervosa Skin and bones appearance; <85% of expected body weight or BMI <17.5 Lowered body temperature and cold intolerance Slower metabolic rate Decreased heart rate, easy fatigue, fainting, overwhelming need for sleep, heart damage Iron deficiency anemia Rough, dry, scaly, cold skin Low WBC count Abnormal feeling of fullness or bloating after eating Loss of hair Appearance of lanugo: downy hairs that trap heat next to skin Constipation from semistarvation and laxative abuse Low blood potassium, leading to heart rhythm disturbances Loss of menstrual periods, leading to increased risk of osteoporosis Changes in neurotransmitter function in the brain, leading to depression Tooth loss with frequent vomiting Muscle tears and stress fractures Treatment of Anorexia Nervosa General Early intervention is crucial for recovery and survival Treatment requires a multidisciplinary team of physicians, registered dietitians, psychologists, and other health professionals May require outpatient therapy, day hospitalization, or total hospitalization Prevention is key Average recovery time is 7 years Nutrition Therapy Gain patient’s cooperation and trust to increase oral food intake enough to raise metabolic rate and reverse physical signs of AN First minimize further weight loss, then add weight (may require as much as 3000 to 4000 kcal/d) Appropriate weight for females is reached when menstruation is restored Multivitamin and mineral supplements, including calcium Reassurance is required as patient will feel loss of control Monitor blood levels of potassium, phosphorus, and magnesium during refeeding RD provides accurate nutrition information, promotes healthy attitude toward food, helps patient learn to heed hunger and satiety cues Psychological and related therapy Reject sense of accomplishment associated with emaciated body Accept themselves at healthy body weight Regain control over other aspects of life Appropriate coping mechanisms for stressful situations Family therapy; family struggles are often at the root of the eating disorder Medications for psychiatric disorders Bulimia Nervosa General “Great (ox) hunger” Episodes of binge eating followed by attempts to purge excess calories by vomiting; misusing laxatives, diuretics, or enemas; or excessive exercise Uses food to cope with critical situations Recognize that behavior is abnormal Low self-esteem and depression Statistics 4% of adolescent and college-age women 10% of cases occur in men Many cases are undiagnosed Body weight is usually at or slightly above normal Female more likely than people with AN to be sexually active Typical characteristics of those with eating disorders (see Table 10-8) Secretive binge eating Eating when depressed or under stress Binging on a large amount of food, followed by fasting, laxative, vomiting, excess exercise Shame, embarrassment, deceit, depression Fluctuating body weight Loss of control Perfectionism Erosion of teeth Purchase of syrup ipecac AN patients frequently crossover into BN behaviors, particularly if parents are overly critical, but BN is less likely to cross over into AN, except in cases of alcohol abuse Binge-Purge Cycle Often have elaborate food rules (e.g., avoid all sweets) Can be triggered by hunger, stress, boredom, loneliness, depression Often followed by strict dieting, leading to intense hunger Binge is self-propelling Does not taste or enjoy food Special time is set aside Usually at night Lasts from 30 minutes to 2 hours Consumption of sweet, high carbohydrate convenience foods Easily and comfortably purged Food could supply 3000 kcal or more When vomiting follows binge, 33 to 75% of food energy is already absorbed When laxatives or enemas used, 90% of food energy is absorbed Many engage in excessive exercise to compensate for binge Afterwards, feels guilty and depressed Physical Effects of Bulimia Nervosa Demineralization, decay, and/or loss of teeth due to repeated acid exposure from vomiting Low blood potassium from vomiting or diuretics, leading to heart rhythm disturbances Swollen salivary glands Stomach ulcers and tears in the esophagus Constipation from frequent laxative use Accidental poisoning from repeated use of ipecac syrup Death due to suicide, low blood potassium, or infections Treatment of Bulimia Nervosa General Experienced, multidisciplinary team of health professionals Weight loss, if present, must be treated before other therapy begins Hospitalization may be necessary First goal of treatment: decrease food intake during binge session Impress patient with seriousness of BN’s medical consequences Nutrition Therapy Establish regular eating habits by self-monitoring Avoid binge foods Avoid frequent weighing Avoid strict dietary rules Regularly consume moderate amounts of a variety of foods from each food group Psychological and related therapy Treatment for depression and high risk of suicide Improve self-acceptance Overcome preoccupation with body weight Correct all-or-none thinking Develop appropriate coping mechanisms for stressful situations Antidepressant medications in conjunction with other therapies Therapy should be long-term because relapse is likely Binge-eating disorder General Recurrent binge-eating episodes During binge, individuals: Eat much more rapidly than usual Eat until feeling uncomfortably full Eat large amounts of food when not physically hungry Eat alone due to embarrassment Feel distressed, depression, or guilt after overeating Prevalence and Susceptibility Not necessarily linked with obesity, but approximately 30 - 50% of subjects in organized weight-control programs have binge-eating disorder (1 - 2% of American population) May be preceded by frequent dieting in childhood or adolescence Heightened perceptions of hunger Half of binge-eaters are clinically depressed and isolate themselves from others Binge episodes are triggered by stressful events, depression, anxiety, eating a “forbidden” food, loneliness, self-pity, anger, rage, alienation, or frustration Food is used to induce sense of well-being or emotional numbness; to avoid dealing with emotional pain and anxiety Often associated with familial dysfunction Treatment of Binge Eating Disorder Nutrition therapy mirrors that for BN Psychological therapy involves identifying personal needs, expressing emotions; and learning appropriate coping mechanisms Eating Disorders Not Otherwise Specified (EDNOS) Partial syndromes that do not meet all criteria for diagnosis with AN or BN Vast majority of those with eating disorders fall into the EDNOS category Other Related Conditions Muscle dysphormia (bigorexia) Characterized by an excessive concern that one has underdeveloped muscles. Most people suffering from this condition tend to have well-developed muscles More common in men, especially body builders Spend many hours lifting weights and performing resistance exercises Suffers exercise with injury and to the point that social relationships and school and work performance are impaired Anabolic steroids or other muscle-enhancing drugs, nutritional supplements are sometimes used Treatment from a sports medicine physician and counselor trained to work with athletes can help individuals overcome this condition Orthorexia From the Greek word ‘orthos’, meaning straight, proper and ‘orexia’ (appetite) Sometimes referred to as the “health food eating disorder” Healthy eating taken to the extreme Spend many hours each day searching for ‘pure’ foods Pregorexia Coined by popular media to describe women who decrease calorie intake and exercise excessively to control weight gain during pregnancy The best treatment will be similar to that for patients with anorexia nervosa Prevention of Eating Disorders Recognize that some concern over diet, health, and weight as well as variations in eating patterns, mood, and weight are normal Treat physical and emotional problems early Treatment of eating disorders is far more difficult than prevention; effects of eating disorders are far-reaching Emphasize overall healthful diet and moderation rather than perfection Caregivers should model positive habits, appropriate expectations, and healthy body image Discourage restrictive eating, meal skipping, and fasting (except for religious reasons) Encourage children to eat only when hungry Promote good nutrition and regular physical activity at home and school Promote regular family meals Provide information about changes that occur during puberty Correct misconceptions about nutrition, healthy body weight, and approaches to weight loss Carefully phrase comments and recommendations about weight Don’t overemphasize weight; promote healthy eating habits Increase self-acceptance and self-appreciation Encourage weight-sensitivity among coaches Emphasize that thinness ≠ better athletic performance Enhance tolerance for diversity in body weight and shape Encourage normal expression of emotions Build respectful environments and supportive relationships Provide adolescents with appropriate, but not unlimited, independence, choice, responsibility, and self-accountability Instructor Manual for Wardlaw's Perspectives in Nutrition Carol Byrd-Bredbenner, Gaile Moe , Jacqueline Berning , Danita Kelley 9780078021411

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