Appetite Summary Notes.docx

Appetite Summary Notes Week 1 Energy Metabolism Basics Food provides chemical energy in the key constituents of carbohydrates, proteins and fats Main Metabolic Pathways Glycolysis, Aerobic, Anaerobic All energy sources can be converted to fat Measuring Energy Kcals as measured by a bomb calorimeter...

Appetite Summary Notes Week 1 Energy Metabolism Basics Food provides chemical energy in the key constituents of carbohydrates, proteins and fats Main Metabolic Pathways Glycolysis, Aerobic, Anaerobic All energy sources can be converted to fat Measuring Energy Kcals as measured by a bomb calorimeter Protein and carbs: 4Kcal/g Fats: 9Kcal/g (energy dense) Alcohol: 7Kcal/g Bodies Energy Needs Basal Metabolic Rate (BMR): energy expended at rest Energy needs based on BMR plus activity Very light: BMR x 1.3 Light: men x 1.6, women x 1.5 Moderate: men x 1.7, women x 1.6 Heavy: men x 2.1, women x 1.9 Most westerners are in the very light to light range Consequences Australian adults are eating slightly more than BMR + activity and so are becoming slowly overweight Carbohydrates Simple Monosaccharides and disaccharides Complex Polysaccharides Function Primarily provide energy Fats (triglycerides) Types Saturated: animal, coconut, palm – increase bad cholesterol Monounsaturated: olive oil, canola – increase good cholesterol Polyunsaturated: vegetable and deep-sea fish – increase good and lower bad cholesterol Transaturated: artificially produced, preservatives, have negative consequences Function Structural, hormone synthesis, fat soluble vitamins, insulation, and energy storage Protein Types All from amino acids, some are essential, and some can be synthesised by the body Function Tissue maintenance and growth, hormone, enzyme and protein synthesis, fluid balance, energy Micronutrients Vitamins Fat soluble: A, D, E, K Water Soluble: C and all the Bs Minerals Most westerners have too much sodium and too little calcium Macrominerals: 100mg/day – calcium, phosphorus, sodium, potassium, magnesium Microminerals: >100mg/day – iron, iodine, fluoride, selenium, zinc (and others) Human Digestive System Gross Anatomy Mouth stomach small intestine large intestine Stomach Receives food in upper part (fundus) – mechanically ground Mixed with stomach acid to form chyme and collects in the antrum After it discharges makes rhythmic contractions (hunger?) Small Intestine 90% of chemical absorption Food triggers release of CCK and pancreatic juices which break down protein and carbs Large intestine Consists of 4 parts Cecum: receives digested matter Colon: removes remaining water and forms B + K vitamins Rectum: temporary storage Anal canal: no explanation needed Water Balance Function All chemical reactions, cellular & interstitial, blood, gut Crucial for energy release and temperature regulation Body loses around 2.2L/day Feeding Strategies What constrains strategies Size, Genes, Habitat Herbivores Eat vegetation, primary energy producers Spend considerable time eating large volumes of food Grazing: grasses are ideal (accessible, widespread, palatable) – have long guts, cutting teeth, specific enzymes, escape strategies Flowers, fruits, and seeds: special colour vision and behavioural flexibility Carnivores Eat herbivores and carnivores, living and dead Most spend little time eating and more time obtaining prey, weight cost to benefit, high in protein so shorter guts Browsing: mollusc, sea slug etc Hunters: actively seek prey Carrion eaters: dead animals or scraps Filter feeders: e.g., whales, have a big mouth and scoop it all up Parasites Obtain energy from a host, needs its host, and gains the most. Cause loss of movement in adult forms, redirection of resources e.g., tapeworm Omnivores Eat vegetation and animals, cockroaches, rats, and humans Advantages: flexible based on scarcity or abundance, rapidly adapt to change Disadvantages: deciding what is safe to eat Week 2 Sensory systems Taste Basics Few qualities but motivationally significant, located primarily on the tongue. Sweet: energy – pleasant Sour: ripeness/vitamin c/fermentation – un/pleasant Bitter: toxicity – unpleasant Salty: depletion and preference – un/pleasant Umami: allergy quackery – pleasant Fat: energy – may have no conscious correlate The Tongue Taste buds grouped into papillae Vallate papillae: 9 in adults, 250 buds/papillae Foliate papillae: 10 in adults, 120 buds/papillae Fungiform papillae: 30cm2(tip) – 8cm2 – mid, 3 buds/papillae (most sensitive) Each bud contains microvilli and lasts 2 days, filled with mucus, may have more than one type of receptor Receptors 2 basic types Ion gated: salt and acid detectors Protein gated: sweet, bitter, umami, fat (each in several forms) The Brain Cell depolarises chorda tympani nerve nucleus of the solitary tract brain stem OR insula + orbitofrontal cortices Insula: primary taste cortex – also emotion of disgust Orbitofrontal: secondary taste cortex Neural Signal to Taste 2 approaches Labelled lines: receptor for A activates only A sensitive neurons (basic qualities) Patterns: stimulus A generates a unique pattern of activity across neurons (more complex qualities) Individual Differences Some could taste PTC, and some could not that split the world into 3 groups Non-tasters: 30% Tasters: 40% Supertasters: 20% - more taste buds, greater sensitivity The common chemical sense Basics Speedy identification and removal of harmful chemical irritants from the skin. Called common because is located over the whole area of the body Located around base of taste buds, cause a reflex response Perception Free nerve endings detect: Temperature: hot/cold Intensity: weak/strong Hedonics: pleasure/pain Spice People have gone to great lengths to secure irritants. Maybe for bland diets, medicine effects, release of endogenous opioids Smell Basics Located at the bridge of the nose and can be accessed orthonasally (sniffing) or retronasally (back of throat) Gross anatomy During certain phases of eating and drinking volatiles ascend via the nasopharynx and bind to the same receptors that are stimulated during sniffing. During chewing when the soft palate (velopharyngeal flap) opens Receptor surface The olfactory mucosa where tissue is bathed in mucus and the ORNs extend microvilli into this region Mucosa function: clear old smells, transport, protection Receptors are G-proteins and chemicals binding result in depolarisation, work by pattern of activation The brain Olfactory bulb olfactory cortex orbitofrontal cortex amygdala mediodorsal thalamus hypothalamus Somatosensation + Proprioception Basics Important in pressure (chewing), texture, astringency Fat Perception Involves texture - greasy, oily, creamy, thin, watery Overall Flavour Taste and smell as a single entity, we always encode flavour information unconsciously Odour-taste synaesthesia Sensation normally associated with one sensory system is experienced when another sensory system is stimulated, most are sound/word-colour, word/flavour are rare, but odour/taste is universal, but people are not aware Brain Information from taste, smell, irritation, and proprioception all converge in the orbitofrontal cortex. Week 3 Thirst Water Resources Fresh water is becoming increasingly scarce at a national and local level. Fresh water is somewhat of a luxury Extremes Dehydration rapidly kills, speed of death depends on environment 2% deficit: strong thirst 3-4% deficit: fit adult can still survive 5-8% deficit: severe fatigue and apathy 10%+ deficit: gross physical and mental deterioration, delirium, coma, death Problematic in children and elderly Homeostatic drinking Body attempts to maintain a set point, behaviour kicks in to regulate consumption when deviations from set point occur Two main types Eating: 1 part water to 1 part food in the stomach and 3 parts water to 1 part food in the intestine for digestive purposes (the set point Blood, plasma and cells: fluid inside and outside the cells. Loss of fluid inside causes thirst and outside can also cause thirst (both further and separate set points) Non-homeostatic drinking Anticipating future water needs Time: some animals prefer to drink at night Anticipatory drinking: most drink when eat, need for water caused by food is not immediate, also – drink while you can Schedule induced polydipsia (SIP): means lots of drinking, free access to water you drink a lot of it (in psychiatric patients, gamblers) if not controlled can be fatal Mechanisms of Thirst Dry Mouth Theory (peripheral) Walter Cannon, when we are thirsty, our mouth becomes dry so we drink Evidence for: saliva levels correlate with water deficits, mouth has to feel water and become less dry for thirst to be assuaged, anaesthetising mouth alleviates thirst Evidence against: oesophagus drinking still get thirsty, people with a lack of salivary glands still drink normally, can account for non-homeostatic drinking Dry mouth is a signal, not a cause of thirst Central Mechanisms An area responsible for thirst should – collect info about water levels in the body and be able to start and stop drinking Hypothalamus Specific cells sensitive to salt levels in blood plasma and reacts to other signals too Saline injected triggers drinking as does electrical stimulation, lesions disrupt drinking Hypothalamus controls release of ADH when loss of fluid from within cells or loss of fluid from blood or plasma which increases water retention and raises BP Problem: probably doesn’t have the ultimate say because it works cooperatively with peripheral systems The Kidney Arterial blood pressure falls as water deprivation ensures and salt levels increase – the kidney detects changes and releases renin; renin causes release of angiotensin which affects CNS (drinking) Blood pressure and thirst Closely linked, high levels of sodium increase BP SIP Appears maladaptive, but not so in the environment. Animals show displacement which is replacing one goal with another Drugs and Food Alcohol Basics Around 90% of people ages 14+ have drunk alcohol and Australia is ranked 23rd in the world in terms of per capita consumption Positive impact Tax revenue, reduction in cardiovascular death, reduces kidney + gall bladder stones, increases bone density, fosters community, pleasurable Negative impact 15% of 20-29 y.o. drink at a rate likely to cause harm, higher rates in indigenous Australians, cancers, CVD, digestive diseases, Injuries, neuropsychiatric disease, costs around 15 billion dollars/year in Australia, most common in drug treatment, crime Metabolism Alcohol is primarily metabolised by the liver, broken down in acetaldehyde then acetate then fed into ACoa pathway. Body can metabolise a maximum of 6-8g per hour Psychological effects Euphoria, disinhibition, reduced anxiety, impaired motor control, increased reaction time, narrows attention, promotes risk taking, enhances aggression Effect on the brain Increases permeability of nerve membranes, acts upon same GABA receptors as anti-anxiety drugs, alters dopamine levels in NA, increases endogenous opioids (liking) Tolerance Two types Acute: within a drinking session, disconnect between BA and behaviour e.g., driving the next day feeling sober but not Chronic: metabolic and tissue, change in the way body metabolises and responds to the same level of alcohol Addiction Problem in around 10% of regular drinkers, 1 in 100 people becomes and alcoholic. CAGE question screening tool – cut down? annoyed by comments? Guilt? Have you needed an eye-opener drink? (Two yesses are a dependency) Neurology Wernicke-Korsakoff syndrome Wernicke’s encephalopathy: dementia, ataxia, visual disturbances Korsakoff’s syndrome: anterograde amnesia, confabulation, language difficulty Caused by poor diet, low thiamine (B1) – Alcohol may interfere with thiamine uptake and metabolic pathways, genetic susceptibility There are other neuro-degenerative disorders and also withdrawal symptoms Mild: tremor, anxiety, insomnia. Moderate: severe tremor, convulsions, hallucinations Severe: delirium tremens Other problems Cardiomyopathy, hepatitis, impotence, sterility, cancer of mouth, tongue, oesophagus, foetal alcohol syndrome Risk factors Parental alcoholism, genetic susceptibility, low sensitivity, abnormalities in DA receptors, abnormalities in 5HT metabolism Drinking culture, comorbid conditions (mental health – self-medication) Treatment Benzos, disulfiram, naltrexone, AA, therapy, relapse prevention training Caffeine Psychological effects Decreases RT, attentional effects, increases alertness, increases feelings of subjective wellbeing Physiological effects Mild diuretic, increase in BP + HR, tremors, anxiety, racing heart How it works Adenosine is elevated while asleep and caffeine prevents it binding to its receptor, interacts with GABA receptors Foods Addiction Some foods are claimed to be addictive, it is because of blame “it is not my fault if I overeat” Maybe sugar, but not fat – changes in the reward system Week 4 Food choice Definitions Preference Relative, would you prefer to eat a stale bread crust or a deep-fried spider Liking Absolute, you would like neither Innate Preferences Sweet Basics A sweet food will almost always be preferred over a non-sweet food, usually signals calories, premature babies preferred a sucrose impregnated nipple to a plain one. Perhaps experience, also context specific. Preference decreases with age Physiology Tongue has one type of sweetness receptor that signals to the chorda tympani, nerve has more fibres dedicated to sweet than any other tastes Periaqueductal grey and NA shell: reward areas rich in endogenous opioids Brain stem ingestive areas: drive reflexive expressions and behaviour Genetic evidence Continued consumption of sweetened food in fructose intolerance, failure to find any difference in sucrose consumption between twins, preference for sucrose can be bred in rats, sucrose liking is reduced in supertasters, all cultures to which sweet food has been introduced continue to readily consume it We are hard wired to like sweet things Salt Basics Salt is an essential part of our diet and lack of it is fatal Salt deprivation Results in dehydration and sensory change – prefer higher salt concentration than before Salt craving Under direct physiological control Evidence: adrenal tumour patient – everything he liked was salty, salt preferences peak in adolescence, greater preference in cold climates, exercise, and salt preference How much do we need? 6g in adults but most consume around 12g – upward effect on blood pressure Longitudinal studies indicate that low salt diets reduce salt preference Salt in food Most excess salt consumption occurs passively: bulking agent (food contains more water – cost reduction), preservative, flavour Bitter and Sour Basics Disgust in babies, probably as a useful safety net Experiential effects Exposure appears to affect preference for bitter, even though it is initially governed by genes Milk Basics Milk is slightly sweet, but no animal consumes milk into adulthood Lactase Enzyme necessary to digest milk, lost at age 2-3 in most humans. Northern Europeans keep it which appears to be genetically based Pastorial societies needed to consume milk to stay alive and Vitamin D assist in absorption of calcium, but production is reduced in Northern latitudes – genetically dominant when needed Personality Basics Strongly heritable, several traits can influence food preference (the big 5, impulsivity) Biological Needs Model Basics Termed the wisdom of the body and is a biological theory of food choice. The idea that our bodies can naturally select a nutritionally complex diet Clara Davis (1935) 15 toddlers reared in hospital until age 4-5, offered a range of nutritious foods – appeared to select balanced diet Limitations: modelling, restricted range Thiamine deficiency in rats Suggested that rats select a diet rich in thiamine if they have been deprived. However, may be from aversion to deficient diet Broadly Not very compelling Scurvy Lack of Vitamin C, took nearly 200 years to discover that lime juice could guard against scurvy – relate to all micronutrient deficiencies Experiential Factors Genes – neophobia Reluctance to try unfamiliar foods – a stable trait that decreases with age Mere exposure could remedy it – learning and perceptual fluency Use of combinations e.g., adding tomato sauce Learned likes Associative learning is a means of changing liking for a food and may occur in several ways Associating a food flavour with calories Associating a food flavour with sweetness e.g., adding sugar to coffee Medicine affect – associating flavour of a medicine with its power Drug-flavour learning – associate flavour with a particular drug related effect (caffeine) Learned dislikes Conditioned taste aversions – typically to unfamiliar foods, can be persistent but not unchangeable, occur irrespective of conscious awareness Social Learning We copy the actions of others, often without intent, likely to be an important means by which children develop food preferences Social-cognitive effect If children had to eat a certain food to obtain access to toys, they really wanted to play with they liked the target food less Growth Getting from milk to adult preferences Cumulative effect, caregiver gives exposure to a range of foods, social learning and TV, peers, some aversions all combined with genetic predispositions Week 5 Food Taboos Basics Nutritious and edible things that a culture does not tolerate as food are food taboos Fall into 3 categories Religious: complex systems of prohibitions Societal: generally specific to a geographical region (e.g., pets) Intra-cultural: typically to woman and children (menstrual cycle, pregnancy, infants) Theories of food taboos Aesthetics Just disgusting, redescription not an explanation Compassion Avoidance of harm to animals – vegetarianism, Buddhism + Hinduism, halal Divine commandment Godly instruction, depends on interpretation Ecology Do not destroy your environment – pigs + cows Health and sanitation Avoidance of parasite and disease Ethnic identity Food defines who you are Natural law A redescription rather than explanation Self-restraint/denial Found in many religions e.g., easter, Ramadan Sympathetic magic You are what you eat Specific Taboos Human flesh In most counties it is not illegal and is not prohibited by the bible, may reflect our basic nature (so obvious it doesn’t need to be said) There is risk but no more so than with other meat It wasn’t always taboo: neolithic cannibalism: evidence comes from genetic resistance to prion diseases, the Cairo famine, Leningrad siege Pigs The only food available for pigs in hot arid climates is food also eaten by people, it probably has an ecological explanation Cows Need to protect both the main source of motive power and valuable protein source (milk) Insects Insect eating is taboo in western cultures, which may reflect the easy availability of protein sources from meat and dairy products Vegetarianism Moral maybe but share considerable attitudinal overlap with green politics, it takes a lot of energy, vegetable matter and water to raise an animal for slaughter and generates a lot a waste. Can the world really afford to eat meat? It may simply be the start of a major social change Starting and stopping eating Hunger Key concepts Hunger The subjective desire to eat and the objective state of the body when nutrient depleted Satiation Loss of desire for food that occurs during an eating bout. Subjectively, reduction in pleasure from eating and increasing fullness. Objectively, multiple neural and hormonal signals that signal the intake of nutrients Satiety The state after a meal, the absence of a desire to eat and physiological state of digestion Measuring hunger and satiety Self-report can be a poor measure, most studies rely on amount consumed, eating rate, food type selected What controls intake Two things Satiety driven: the amount you ate at the last meal, time blind humans are satiety driven Hunger driven: the longer you are without food, the more you eat at the next meal, when time cues are available Short vs long-term intake Especially pertinent in small mammals, many different mechanisms control Controlling Food Intake Peripheral Factors Contractions Stomach contractions happen when the stomach is empty, do they cause hunger? People without a stomach can and do feel hunger, same as gastric banding, there is only a weak relationship between stomach contractions and hunger, they are a signal that the stomach is empty, like dry mouth theory Cues Environmental cues can trigger hunger, sounds, smells or sights. If they influence behaviour this may be important in triggering eating. Probably via associative learning – what level can environment affect behaviour? Portion Size The amount of food on your plate will influence how much you eat Variety The more choice, the more you will eat (satiety, excitement, alcohol) Accessibility More accessible increases consumption – we are lazy Time Expect food at a particular time, we learn mealtimes as a social construct Temperature Ambient temperature and temperature regulation, as body temperature drops, you become more hunger because digestion warms you up People Most consistently powerful, the more people there are, the more food gets eaten per person. Most pronounced for family members, then friends but also work for strangers, no gender effects, occur for any meal or snack Distraction People eat more while watching TV, just watching TV can trigger eating, can also have delayed effects – harder to remember what you have eaten Mouth Sensory factors, sweet foods in greater quantities Guts Intragastric feeding (food straight into the gut) – reduces sham feeding, nutrient density hastens satiety Digestion Chemicals released into the blood stream seem to be the most promising candidate for controlling termination of eating Week 6 Starting and Stopping Eating Theories of Eating Glucostatic Theory Mayer 1950’s: blood sugar level drops before a meal and rises after. When BSL high in Arteries but low in veins we were not hunger When BSL low in Arteries and low in veins we were hungry If you inject insulin during inter-meal period hunger ensues If you reduce BSL by 50%, caloric intake increases by 200% BUT Good in the but what about long term? Lipostatic Theory Developed to deal with long term, key idea that the body has a set point and if we move from the set point the body works to restore it – homeostasis Fat Lipostatic theory suggests that if we exceed fat set point then we work to reduce fat and vice versa – the most important indicator is leptin Leptin White fat cells secrete leptin – the bigger it is the more it secretes More leptin is associated with inhibition of hunger and stimulation of satiety (doesn’t work in morbidly obese) Leptin receptors in the hypothalamus (key brain area involved in appetite) Follows a circadian rhythm – highest at night How do the theories fair? Lipostatic pretty good, Glucostatic not so good Insulin A hormone released by the pancreas that regulates glucose metabolism – forces storage as glycogen – BSL is closely regulated by insulin Type I Diabetes Absence of insulin production – high BSL, leads to neuropathy, blindness, renal failure, and heart disease Type II diabetes Cells become insulin resistance – linked to body mass Affects Raising insulin before a meal can trigger hunger – preparing for an influx of nutrients Raising levels of insulin during a meal can reduce food intake – seemingly paradoxical, but rising levels normally signal an influx of nutrients Cellular Glucose Metabolism Hypothalamus Glucose metabolism within cells in the hypothalamus may be an indicator for short term energy needs. Monitors current energy needs but unlikely to control it Biological system May be crucial at the extremes, day to day though, it is a combination of multiple psychological and biological processes Satiating Agents Basics As food moves from stomach to the small intestine – it could influence satiation Criteria Must be released during feeding Exogenous administration must affect feeding Exogenous dose must match endogenous does The agent should act and clear rapidly The effect should not be due to other causes CCK Released by the SI – stimulates the gall bladder to contract – the more CCK released, the slower the stomach empties Higher protein and fat levels increase CCK and elevating levels reduces food intake – meets criteria Glucagon Released by pancreas and increases level of blood glucose – opposite to inulin – released shortly after feeding starts Modes of action Plasma CCK brain receptors CCK binding to vagus nerve (hypothalamus) Plasma CCK Liver function Glucagon via the liver Food Types of food varying by caloric density and nutrient type Fatty food: reduces intake in the short term but insensitivity in the long term Low calorie food: people eat more, may be associative learning Nutrient type mediates – protein more filling than carb – appears to be mediated by the SI Texture mediates – solid more satiating than liquid – rate of gastric emptying, stomach tension, speed of contact between nutrients and digestive processes (faster for liquids), crunchy is more satiating Central Mechanisms Craniopharyngioma 9% of childhood brain tumours, present with either obesity or emancipation, removal may cause hypothalamus damage leading to lifelong problems with weight regulation (hypothalamus may be home to various ‘centres’) Hypothalamus lesions Rats demonstrated hyperphagia and became obese Lesions in the Ventro Medial Hypothalamus (VMH) induced hyperphagia (remove brake) Electrical stimulation of VMH inhibited eating (apply brake) – VMH as satiety centre? VMH Certain cells sensitive to BSL Lateral Hypothalamus (LH) If lesioned, rats die of starvation (remove accelerator, if stimulated rats eat (apply accelerator) Stellar’s theory (1954) VMH is a satiety centre (brake) and LH is a hunger centre (accelerator) in conjunction with other brain areas and peripheral factors Problems It may be because of something else (arousal, sensory processing, motor behaviour), the lesions were crude and more specific lesions are far less effective, many additional brain areas involved (hippocampus, temporal lobes, anterior cingulate cortex etc.) Eating and Memory HM Inability to code new memories, can’t remember his meals, kept eating Issues Control of eating may be under cognitive control Neurochemicals Neurotransmitters Serotonin and Dopamine, raising levels of SE and DA in the LH reduces meal size, raising levels in VMH reduces meal frequency Serotonin: induce satiation and satiety both centrally and peripherally Neuromodulators Neuropeptide Y increased in the hypothalamus increases eating, long term causes obesity Intracerebral corticotrophin releasing hormone (CRH) appears to alter set point via receptors in the hypothalamus – CRH regulated by leptin, more leptin = more CRH – reduced food intake Ap-A-IV increase is associated with reduced appetite – indicates nutrient density Interactions of periphery and central Fat and Hypothalamus High levels of leptin alter function of hypothalamus reducing food intake CCK – Vagus – VMH CCK released in the intestine affects vagal function and hence activity in the VMH reducing food intake Boundary model Presumes that most of the time eating behaviour is controlled by psychological and environmental variables but biological provides the boundary conditions Week 7 The food system The food system includes all the processes that take place from farm to plate The past Industrial Revolution WW1 Chronic malnutrition For every 1000 infants, only 200 reached age 50, only 100 reached 70, most dead before age 5 Most dependent on wheat – fluctuations correlated with mortality rates in cities Consequence of chronic malnutrition – compromised immune system The Present Western Countries Chronic malnutrition is rare because food is secure and cheap Food Supply Problems Cost of food Between the 17th and 19th century, 80% of income spent on food 1900-2003 – dropped from 42% to 13% There are 2 ways to address high price of food Drive the cost down Drive wages up Food security Food supply more fragile 17th to 19th century Irish potato famine: bad weather and fungus destroyed the crop, between 1845-52 Irelands population dropped by 25% Could be solved by Improved agricultural practice Reliance on national and international sources Food supply Solutions Farming practices improved with mechanisation The Rotherham plough: more efficient at cutting, lifting, and turning soil (more land cultivated) The seed drill: reduced labour for seed sowing, reduced volume of seed needed to be sowed Threshing machine: mechanised separating wheat from chaff 4 crop rotation system 1730 rotation of crops that best suited season and soil which reduced pests, increased fodder for livestock and manure was used on the fields Green revolution 1970s Reliance on oil-based products – pesticides, fertiliser Food preservation Pre 1800s – salting, drying, and smoking After that more technologies were developed Canning: 1806 in glass jars and a combination of heating and vacuuming were used to preserve food Freezing: adopted in 1830s, applied to meat, cheese, butter, and milk in refrigerated ships in 1877 Cooling: large storage facilities to keep crops for many years Chemical: nitrate to preserve meat products Bulk transport The train! Saved Europe from famine in 1870 – allowed development of international trade in basic food stuffs The present problems Capitalist model Requires continued growth Growth How can we continue to grow profits Value adding: e.g., processed TV dinners instead of just staples, increasing choices and opportunity to eat Advertising: we are continuously encouraged to eat Consolidation: bigger players absorbed smaller players – makes efforts at reform difficult Hidden Costs Soil degradation, extensive use of fossil fuels in delivery + production of fertilisers and pesticides, excessive use of agro-chemicals, reliance on limited plant/animal varieties + loss of biodiversity, animal welfare concerns, disposal of agricultural wastes and water use Distortions The market for agricultural products is not fair, especially in third world countries – they are encouraged to grow cash crops to pay their accumulated debt (must import basic food stuffs) Food security is also a problem Paradigms The productionist paradigm What we have been looking at so far The life sciences paradigm Concentrates on scientific solutions to the ecological and agricultural problems The ecologically integrated paradigm Concentrates on more human centred solutions such as organic farming, agricultural development, and localised production Week 8 Obesity Fat cells We have 2 types Brown Fat Cells (BAT): generate heat, located either side of the spinal column, rich in mitochondria and not implicated in obesity White fat cells: insulate the body, cushion internal organs, long term energy store, endocrine function (leptin, resistin, adipose factor) White Fat cells 20% of a woman and 15% of a man, distributed in different ways Positive energy balance: ingest more energy than we use, creates white fat cells obesity Measurement BMI Divide weight in kgs by height squared in metres >18.5: underweight 18.5-24.9: normal 25.0 – 29.9: overweight 30+: obese Pros are that its easy, can be measured remotely, accurate and correlates with adiposity Cons that it takes no account of fat distribution, no account of muscle mass, influenced by age and trunk to leg length Skin fold thickness Stomach and top of arm/leg, no measure of adiposity and hard to define Waist circumference Good for estimating risk factor for heart disease and stroke but doesn’t provide measure of adiposity and difficult to define Bioelectrical impedance Estimates % body fat by resistance of electrical flow, sensitive to hydration and is only a rough measure Statistics Prevalence We are amid an obesity epidemic USA Getting more obese through the decades, impacted by age, ethnicity, and SES, also greater in children and adolescents OECD Also increasing obesity especially in USA, England, and Australia. Not as bad in Canada, Spain, and Austria Australia 67% overweight and 31% obsess (a big increase since 1989) At age 4, 15% overweight and 5% obese At age 10, 20% overweight and 6% obese The greatest in regional areas Health Care Costs Australia 10.7 billion dollars per year US Direct health care costs for the obese have risen from 52 billion US dollars in 1995 to 178 billion dollars in 2012 Medical Consequences Diabetes Type 2 – insulin dependent diabetes is now very common (around 1.5M Australians). The body still secretes insulin, but cells are insulin resistant – resulting in hyperglycaemia If poorly managed results in microvascular and macrovascular diseases Heart disease, hypertension, and stroke Obesity raises blood pressure and increases levels of bad cholesterol resulting in atherosclerosis – blockage of coronary artery Obese person has a 3-fold increased chance of a heart attack Cancer Obese people are 23% more likely to die from cancer than individuals of normal weight Cancer detection and treatment is more difficult in obese individuals leading to higher mortality Osteoarthritis Degenerative diseases of weight bearing joints Reproductive disorders Increased risk for pregnancy and of neural tube defects in the foetus and impotence in men Sleep apnoea Fat on the neck and face and stomach when sleeping can stop breathing and lead to elevated risk of heart failure Psychosocial Effects Children and young adults Viewed by peers as more lazy, dirty, stupid, ugly, and dishonest, poorer educational and social outcomes than other chronic conditions, anxiety and depression are far more common than in chronic pain, cancer, and quadriplegics Adults Less likely to marry, earn less money, have fewer educational and career opportunities, lower quality medical care Week 9 Obesity 2 The Causes Basic Energy intake outstrips energy expenditure 2 key factors – the development of obesogenic environment + genetic predisposition The obesogenic environment Developed over the last 40 years and most evident in industrialised nations Characterised by reduction in physical activity (PA) and increase in availability and consumption of processed foods Physical activity Last 40 years reduced PA through increased car usage and TV viewing Digital media has created several sedentary leisure activities Occupation: became less physically demanding Travel to work: less than 10% now made on foot or bicycle, more primarily reliant on the car Leisure activity: the main one now is TV (26hrs/week)- pronounced in children and associated with snacking (also ads) Evidence suggests an association, overall, less PA contributes to higher rates of obesity School 1980s USA there was a drive to cut costs – loss of exercise programs, sale of playing fields, fast food in canteens, fast food advertising in schools, exclusive soft drink contracts – similar in the UK Demographic Shifts Many families have all adult members working – greater reliance on processed foods Processed foods Highly palatable, large quantities of fat, sugar and salt (in the form of trans-fat) Soft drink consumption is independently associated with obesity Variety Rats given a large quantity of palatable foods become obese and humans are similar – palatable foods are available everywhere always and supermarket stock a large variety with new foods constantly coming online Portion Size Has increased – consumption increases Supersizing: marketing ploy where small extra cost is accompanied by extra-large portion size – profitable Is it the environment? Evidence is strong that it is Pima Indians: In US high obesity, in rural Mexico lower rates with the main difference being diet and exercise (not genes) Migration studies: US migrants have higher BMIS than their relatives in country of origin Genetics Susceptibility Genetic influences on bodyweight are ‘polygenetic’ Twin, adoption, and family studies show an increased risk of obesity if person’s relatives are obese Predisposition Energy balance: thermogenesis, liver metabolism of fat Feeding behaviour: fat preferences, leptin resistance, craving Skeletal muscle growth: rate of growth Satiety regulation: serotonin levels, POMC levels Fat cell numbers: Obese individuals may be born with more Criticisms Excess mortality *Excess mortality does not occur until you get into the obese range Yes, BUT increasing BMI associated with risk of chronic diseases such as diabetes and heart disease BUT does seem to enhance survival if you are physically fit Criticism ignores – reduction in quality of life, social and financial burden, obesity comes from progressive weight gain over time Shorter Lives *Projected death rates from obesity are overstated (this generation will live longer than the last) We may become better at keeping people alive with complications, however no generation have ever encountered obesity and Type II diabetes at the rate observed today Causes *The focus on environmental factors is too simplistic Critics argue that too much food and not enough exercise do not adequately explain why we are getting fatter True, their importance might have been overstated Other correlates Less sleep Maybe, several recent findings suggest that lack of sleep may precede obesity Linear relationship between amount of sleep and weight gain, sleep deprived eat more, sleep deprivation alters metabolism by reducing plasma leptin and increasing ghrelin Climate control People in cold and warm countries are more likely to live in thermoneutrality, bring hot and being cold require energy, nobody knows if this contributes Quitting smoking Ex-smokers tend to gain weight and over the last 30 years people who have quit smoking has gone up. It is still better to give up, you would have to gain 45kg to equal the risk of dieting from continuing to smoke Pregnancy Maternal metabolic abnormalities during pregnancy increase obesity risk later in life, overweight mothers are more fecund, mothers are getting older and having an older mother is a risk factor for overweight and obesity Chemicals Certain drugs cause weight gain and chemical pollutants Week 10 Obesity 3 Treatment of Obesity Diet Most obvious strategy – reduce intake – choices range from evidence based to farcical but all work in the same way, by a negative energy balance to burn fat supplies No matter what is being modified, to be effective a diet needs to be around 1500Kcal/day Evaluating a diet Success is defined as a loss of 5% initial body weight at one year Fat Reduction Diets Fat is the most energy dense macronutrient, therefore reducing a by a gram of fat has more effect than any other macronutrient Low fat diets have been the traditional approach medically 3 large scale trials – being defined as 20% of intake is fat (30g a day) – and they work Very Low-Fat Diets For morbidly obese e.g., optifast Reduce energy intake from fat to less than 5% Result in larger initial weight loss, but weight regain may make them no more efficient long term than low fat diets Mediterranean Diet Good fats predominate, high in fibre, main energy from low GI carbs, limited red meat and lots of fruit and vegetables Very few clinical trials but epidemiological studies suggest this type of diet is associated with lower risk of heart disease, longevity, and better cognition High Protein diets Up protein levels at the expense of fat and especially carbs e.g., paleo Far fewer studies and none that meet criteria – one study, high protein group lost more than low protein group but after 2 years there was no significant difference High protein group demonstrated a notably greater reduction in abdominal fat (maybe also extra weight loss from greater satiation) Low carb diets Reduce carbs and up protein and fat intake e.g., Atkins diet Several studies show they are as effective as low-fat diets but they have an edge (safety concerns – not well understood) – compliance is easier because they tend to restrict foods that contribute less to meal enjoyment Low GI diets GI is the rate at which blood sugar rises following carbohydrate intake – a good with GI of 100 is one which raises BSL at the same rate as glucose (white bread, mashed potato) Carbs with low GI are considered healthier Only limited diet effectiveness *all small sample sizes – may help metabolic disorders and cardiovascular complications What predicts weight loss Length of treatment phase Single best predictor, compliance becomes a problem with long programs, face-to-face contact needed Maintenance Absolute gains are around 3-4% of initial body weight lost at 4 years Multicomponent treatment Combining diet with therapy Motivation enhancement Monetary motivation does not help Relapse prevention Possibly helps, not very successful Health Promotion Thinking differently It is an environmental problem first rather than individual PA Increase it, 70% of Australians do too little or no exercise Limit child commercialisation Stop advertising to children – the average child sees 1000 junk food adverts on TV/year Food and soft drink in school Provide health foods + reduce access to soft drink Reduce portion size A super serve of fries provides 30% of daily energy needs, yet there are no incentives for consuming healthy food Change price structure Junk food is cheap and available – unlike fruit and veg Week 11 Obesity IV Treatments Exercise May increase weight loss, improves glucose tolerance + BP, increases lean body mass, improves diet compliance, improves mood CDC and US Surgeon general suggest 30 mins of moderately intense PA per day, I of Medicine and IAS of obesity suggest double Moderate intensity is HR of 55-69% of Max HR 70-75% of adults do not meet CDC guidelines because it is difficult to initiate and maintain – can be remedied by behaviour therapy and lifestyle programs Behaviour therapy Identify behavioural factors that promote problem behaviours and prevent uptake of healthy behaviours Treatment components of self-monitoring, stimulus control, cognitive restructuring, and time limited therapy sessions (group format better) Behaviour therapy alongside diet is better than diet alone in the short term – long term is not currently known Medication History not very reassuring Amphetamines: dependence/tolerance – not used since ‘70s Dexfenfluramine/Fenfluramine: pulmonary hypertension side effect Rimonabant: increased anxiety, depression, suicide Sibutramine: increased risk of heart attack and stroke One major advantage – less reliant on self-control Currently there are 2 main approaches: centrally acting drugs + peripherally acting drugs To be classed as effective, medication needs to reduce weight by more than 5 or 10% - relative to placebo Centrally Acting Drugs Phentermine – used for over 50yrs, effect the hypothalamus where it binds to TAAR1 receptors causing reduced hunger, may be prescribed with topiramate Peripheral drugs Orlistat – blocks pancreatic lipase resulting in a failure to digest (around 30% of) fat, highly adverse consequences of eating fat, independent improvements in blood lipids, less effective than Phentermine Surgical Treatments Restrictive procedures Gastric banding: reduce volume of the stomach by staples, 30-50% of initial body weight lost at one-year, low morbidity and reversible (side effects: gastric reflux, solid food intolerance, ulcers, and hernia) Vertical sleeve gastrectomy: restrictive and irreversible but with added benefits, performed laparoscopically, effective in children Malabsorptive procedures Shortening small intestine: varying length of SI, not generally used Roux-en-Y gastric bypass: stomach reduced in size + new stomach pouch exits to SI + old stomach connected to new SI, smaller SI restricts absorption of food, rapid benefits to type II diabetes and alteration in food preferences (patients need continuous medical supervision) – gold standard Other Weight loss Body dissatisfaction Dissatisfaction in what one imagines one looks like, comes in 3 forms Distorted body image: I am fat As a discrepancy from ideal: I think I am larger than I’d like to be Generally negative appraisal: I don’t like my body Perceptions can be measured by projection measures, computerised morphing, perceived vs ideal body shape, negative thoughts questionnaires Who is dissatisfied 50-75% of women, 30%+ of men, appears in females at 8 or 9 years old More common in westernised, higher SES, acculturating migrants Why The media – thin women and muscular men portrayed as the norm The family – daughter reflect mother’s level of dissatisfaction Maybe preoccupation with thinness toward a sexual ideal, physical attraction is a common motive for losing weight (foot binding, corsets, slimness + bikinis in the 60s) The Psychology of dieting Central concept of restrained eating – restrain or exert control over body size and food intake Restrained eating The what the hell theory: dieting leading to weight gain rather than weight loss (overcompensation, one bad thing a heap of bad things) Starvation Demographics World population 1B malnourished, severe 0.5-2%, milder forms – up to 50% Children may be adversely affected, Asia and Africa have the highest incidence Definitions Chronic: the norm, causes studing, with exacerbations under famine Acute: causes wasting Famine Broadly categorised into 2 Human catastrophes: genocide, war, social unrest, poverty, poor gov etc. Natural catastrophes: plagues, tempests, flooding, drought Pure examples are rare, most are a combination of both Consequences of famine The moral economy reduced food intake and meal spacing use of wild foods sale of non-essential possessions sale of all possessions migration (slums or refugee camps) Psychological effects Children suffer more than adults, women and older children are often the last to die Children Protein energy malnourishment (PEM) Marasmus: diet insufficient in calories – extreme underweight, irritable, apathy, shrunken, chronic diarrhea Kwashiorkor: sufficient in calories, insufficient in protein – edema and sores Long term effects – 50% of PEM sufferers have an IQ <90, also attention and STM problems Pregnancy Spontaneous abortion, reduced brain weight and number of neurons and glia, irreversible, raised BP – proneness to diabetes and heart disease Adults Impotence in men, eliminates menstrual cycle in women, loss of lean + fat body mass, lowered HR + basal metabolic rate + BP, edema, lethargy, hypersensitivity to cold, impaired immune function (kills) Long term psychological effects Far more likely to binge, extreme reactions to throwing out food, storing excess food, difficulty lining up for food, anxiety if no food available, craving carbs Week 12 Eating Disorders Anorexia Nervosa (AN) Clinical Definition Restriction of energy intake leading to significant low body weight, intense fear of weight gain, disturbance in perception of shape of body weight Subtypes Restricting: dieting, fasting, and exercise Binge-eating/purging: vomit, laxative, diuretics, and enemas Specification Full, partial or in remission and severity based on BMI Prevalence Lifetime – 0.5-2% in women (women 10-20:1), predominantly in middle- or upper-class Caucasian women High rates in dance, fashion, and elite sport, typically appears around 12-13 years old (range 10-60) Onset Starts with minor diet changes increasing focus on safe foods thinness starts to become the only goal Medical consequences Overactivity, cold sensitivity, multiple endocrine abnormalities, low BP + HR, diminished libido, osteoporosis, neurological impairments (reduction in hippocampal volume), anxiety and depression Mortality 5-10% from starvation and suicide Cause Not clear, interacting factors of genetic, biological, psychosocial, social and cultural variables Genetics Female relatives of someone with AN are 7-20x more likely to develop Serotonin metabolism abnormal, OCD like personality characteristics, abnormal satiety, chronic anxiety Diminished sensitivity to hunger cues, heightened sensitivity to reinforcers, tendency toward excessive exercise Development 25% of parents of a child who goes on to develop AN have experiences a major obstetric difficulty and loss compared to 7.5% of matched controls (overprotective?) – parents of children with AN have higher anxiety, abnormal attachment styles Prematurity and birth trauma 2-3x higher HPA Axis The hypothalamus (PVN) releases AVP and CRH pituitary glad releases adrenocorticotropic hormone affects adrenal gland which releases cortisol that supresses PVN (also regulated by SE pathways and hippocampus feedback) Stress results in the activation of HPA – rising cortisol – raises blood glucose, increase BP and down regulates immune function HPA function is abnormal in AN – profound changes in HPA in puberty – window of vulnerability Hypothalamus is involved in appetite regulation – chronic release of CRH can affect appetite regulation Maintenance Highly treatment resistant, process of weight loss may become physically addictive, evidence of heightened b-endorphin levels Outcome 50% never fully recover and experience repeated relapse Treatment First goal is refeeding which takes place in hospital under strict supervision Combined with ongoing psychotherapy Additionally – antidepressants Bulimia Nervosa (BN) Clinical definition Recurrent episodes of binge eating + recurrent inappropriate compensatory behaviour to avoid weight gain, both at least once a week for 3 months Self-evaluation influenced by body weight and shape Independent of any episodes of AN Specification Full or partial remission and degree of severity defined by frequency Prevalence Lifetime 1-3% in women (ratio 10:1) Typically develops in late adolescence or early adult hood, same cultural and social groups as AN Medical consequences Dental erosion, swelling of parotid glands, electrolyte abnormalities, rare complications from oesophageal tear/gastric rupture Cause History of AN, childhood and parental obesity, history of dieting, family environment (critical comments, sexual abuse), higher rates of anxiety and depression, personality disorders, substance abuse + self-harming, traits of impulsivity Maintenance Physiological changes related to abnormal satiety Enlarged gastric capacity, delayed gastric emptying, reduced gastric elasticity, impaired CCK release, impaired CCK release, reduced vagal information flow, abnormal SE function and serum leptin levels Prognosis 50% full recovery, 30% occasional relapse, 20% chronic Treatment Combination of CBT and antidepressants (more easily treated than AN)