Biological Psychology - MOTIVATION AND EATING
What is the prevalence of anorexia?
-1-3% of all women affected -Average age 18-20yrs -Most common in higher social class white and asian women (16:1)
What is the prevalence of bulimia?
-1.5% women and 0.5% men sufferers in the USA (with increasing prevalence) -Harder to diagnose than anorexia as often normal weight
What are the characteristics of anorexia?
-15% below average weight and experiencing over 2yrs of extreme dieting -2 types are restricting and binging -Fear of fatness, body image disturbance, high levels of exercise -10% likelihood of death and high rate of suicide (with high relapse rates) -Comorbidity with OCD and depression e.g. food rituals, isolation
How are serotonin and dopamine levels implicated in eating?
-Food elicits strong dopamine and serotonin bursts which elicits reinforcement and provides a hedonic effect -Serotonin is derived from tryptophan (amino acid linked to carbs) -When we see food we get a release of serotonin which increases as we eat thus suppressing our appetite -Abnormalities in serotonin and dopamine levels are linked to eating disorders e.g. depression > BUT McIntyre et al (2006) found that 19% of depressed people are obese and 15% of non-depressed people are obese so there is no direct link
What are the 2 theories of anorexia?
-HYPOTHALAMUS DYSFUNCTION - disturbed hypothalamic function means lack of weight thermostat and abnormal levels of hypothalamus NPY (stimulates feeding behaviour) are present -BIOCHEMICAL IMBALANCE OF DOPAMINE - possess high levels of homoyanillic acid (waste product of dopamine) so do not have the same incentive to eat certain foods
What is a drive?
An unpleasant state of arousal/tension caused by a need which impels the organism to engage in behaviour that will satisfy the need and reduce tension
What evidence is there to suggest ghrelin is important in inspiring motivation to eat?
Animals who have had food prevented from moving from the stomach to the intestines experience constant satiety (Deutsch, Young and Kalogeris, 1978)
What is the leaky barrel analogy of metabolism?
Argues that metabolism is variable depending on how much food is coming into the body > balance rate of water leaking from the barrel (energy expenditure) with water coming in (available food)
How do we know that gastric distension is not the only factor informing when we stop eating?
As we are still able to feel full when we haven't had enough calories and if we are eating something that tastes nice (e.g. chocolate) the satiety signal is suppressed > CCK and gastric distension work together
What are the 2 interpretations of why animals with lesioned ventral medial hypothalami become obese?
INITIAL INTERPRETATION: Lesioned animals become obese because they overeat NEW INTERPRETATION: Lesions lead to increased insulin which causes more glucose to be stored and a decrease in the breakdown of lipids SO not only is the rat eating more but it not using some of the stored fat > Leads to altered set point
What are the 3 hormones involved in eating? What happens to their levels when full and when hungry?
INSULIN, LEPTIN AND GHRELIN High glucose insulin release and high lipid leptin release = full stomach Low glucose insulin release and low glucose leptin release = empty stomach > release ghrelin
What is maintenance of homeostasis?
It involves deviation of a parameter from the normal values followed by a corrective action associated with motivation (instinct, drive) SOCIAL HOMEOSTATIS is the maintenance/regaining of contact with "special others" (partner, child, parents)
What did the chocolate craving study show?
(Rolls & McCabe) -Comprised both cravers and non-cravers as subjects and involved the sight, flavour and combination of chocolate -Found that key areas at the front of the brain (linked to rewards) responded more in cravers compared to non-cravers -Sight of chocolate produced more activation in cravers' medial orbitofrontal cortex and ventral striatum -Picture and flavour induced greater effect than the sum components on medial orbitofrontal cortex and pregenual cingulate cortex -Pleasantness ratings correlated with brain response in these areas > Biological differences exist in how we respond to certain foods
What are the 5 major motivation theories? Which of these are less well defined/older?
*INSTINCT THEORIES - Human behaviour is motivated by instinct that is innate (e.g. hunger) and which are activated by environmental stimuli *MASLOW'S HIERARCHY OF NEEDS - When different motives compete, basic survival needs to be satisfied first before we are motivated to satisfy higher level needs *AROUSAL THEORY - Behaviour is motivated by the need to achieve optimum levels of arousal dependent on the individual e.g. state of alertness, mental/physical activation DRIVE REDUCTION THEORY - Motivation originates from biological needs to maintain the body in a state of balance or equilibrium INCENTIVE THEORY - Behaviour is motivated by intrinsic and extrinsic incentives or rewards *First 3 are less well defined and older theories
What does set point theory suggest about how humans maintain the same body weight?
-A drive reduction theory arguing that we have a set point for our body weight and for how much we eat SO as adults we broadly maintain the same body weight year on year -Hypothalamus monitors the storage and use of carbohydrates (GLUCOSTATIC THEORY: monitors glucose from food consumed in the day) as well as the storage and metabolism of fats (LIPOSTATIC THEORY: monitors fat stored from food consumed in the previous week, we fluctuate across days so may eat slightly more/less next day as a consequence)
What is the difference between anabolic and catabolic metabolism?
-ANABOLIC occurs during the prandial state (when the intestines are full and the blood is filled with nutrients) and involves storing energy as glycogen (in liver and skeletal muscle) and triglycerides (in andipose/fat tissue) -CATABOLIC occurs during the post-absorptive state (fasting condition when the intestines are empty) and involves the breakdown of glycogen and triglycerides to supply the body with fuel for cellular metabolism
What is the relationship between insulin and glucose?
-After a meal excess energy (glucose) is stored as glycogen triglycerides and as we become hungry again we use this stored energy to maintain glucose level -Insulin is a PROTEIN HORMONE released when there is an increase in glucose to regulate the amount in the blood -Insulin is the key allowing glucose into cells to be used as energy -Glucose is elevated when insulin is reduced and glucose falls when insulin rises
What issues do lesions to the lateral hypothalamus cause?
-Aphagia (absence of eating) as if food were distasteful > linked to anorexia -General lack of responsiveness to sensory input (not just food or drink) -Problems digesting foods as LH also controls autonomic responses like digestion secretions
What is positive incentive theory?
-Argues that we are not just driven to eat by energy deficits but also because we crave it (anticipated pleasure of eating provides positive incentive value) -Incentives are dependent on current homeostasis e.g. hunger/satiety level, individual differences in listening to interoceptive signals
What are the criticisms of Maslow's hierarchy of needs (1943) theory?
-Assumes self-actualisation (at the top of pyramid, to do with achieving very best) is the end goal which is very Westernised as not all cultures value the self so highly e.g. might argue community/relationships more important -Untestable (how do we know we move through this hierarchy?) -Assumes we move from one step to the next but we move between levels/fluctuate depending on our ultimate goal at that moment
What is the breakdown of energy expenditure in the human body?
-Basic metabolic rate (expended over time at rest) accounts for 70% of energy expenditure -Physical activity makes up 20% -Diet-induced thermogenesis (expended in processing food for use and storage) makes up 10%
What are the characteristics of bulimia?
-Binge eating alternating with strict diets -Purging -High comorbidity with anxiety, depression and OCD
What are instincts?
-Complex, unlearned behaviours that have a fixed pattern throughout species -Disposition towards responding in a particular way when confronted with a specific stimulus -Unlearned, innate and automatic
What factors influence positive-incentive value?
-Current glucose levels (normal range?) -Knowledge/learning about food e.g. mad cow disease or previous food poisoning might cause an aversion to food -Food smell and anticipated flavour -Presentation of food -Social situation > Incentive theories recognise there are many factors influencing hunger and eating (unlike drive reduction theory)
What are the limitations of instinct theories?
-Difficulty testing this theory as there is no clear definition of what an instinct is -Humans are able to adapt eating behaviour so motivation may not always be instinctive e.g. might decide to eat before/after attending lecture
How effective is hormone replacement in treating obesity in humans?
-Does not work so effectively in humans as in mice as many injected with leptin fail to respond due to decreased sensitivity to leptin (rather than lack of it) causing their obesity despite producing plenty of leptin (harder for it to cross the blood-brain barrier) -Decreased sensitivity to leptin can also be seen in pregnancy and during hibernation (when increased food intake makes sense) -Over-eating damages the part of neurons of hypothalamus leading to decreased sensitivity BUT this can be undone with exercise which helps to repair cells
What similarities can be drawn between obesity and addiction?
-Evidence suggests obese people have fewer striatal D2 (dopamine) receptors similar to cocaine addicts -Food acts like a drug, bringing pleasure, reinforcing and becoming a motivator for consumption (overrides homeostatic mechanisms) BUT many argue against this hypothesis
What have animal studies shown us about social influences on eating habits?
-Hepper (1988) fed garlic to pregnant rats and found that pups given 2 dishes (onion vs garlic) preferred the dish containing garlic > Prenatal environment is important -Bronstein et al (1975) found that weaning rat pups enhanced preferences for foods eaten by mother -Wyrwicka (1978, 1981) trained cats to eat unusual foods (e.g. banana) and found that the weaning kitten ate the food the mother had been eating = imitation
What evidence is there showing the evolutionary advantage of fluctuations in insulin and glucose?
-Humans have been shown to eat more in Autumn (de Castro, 2000) perhaps to prepare for winter with less food -In autumn, animals that hibernate have higher insulin
What happens to the availability of glucose before/after we are eating a meal?
-In anticipation of food, insulin is released and blood glucose drops = increases drive to eat -When food enters stomach, insulin secretion is stimulated further and it is maximal when food is stored in the intestines -Rise in insulin is a satiety signal which acts directly on the arcuate and ventromedial nuclei of the hypothalamus -If insulin remains high the body continues to move glucose into cells (glycogen and triglycerides are broken down to provide the body with a continuous supply of molecules used as fuel) > glucose drops -Despite high insulin hunger increases due to the drop in glucose
What have parabiosis studies of mice shown about obesity?
-In lab where mice were being studied it was noticed that some mice became fatter than others which led to identification of an obese ("ob"/leptin) gene -ob/ob mice (lacking both copies of gene ob) didn't produce leptin which led their brains to respond as if they had no fat stores and is starving = conservation of energy and higher food intake -Injected leptin into these mice caused them to lose weight -When mice with the "ob" gene were parabiosed to normal mice the ob mouse ate less and obesity reduced as if the missing hormone was replaced (Coleman, 2010) > Obesity can be reversed through hormone treatment (increasing leptin)
How did Grill and Betteridge (1985) show that taste is affected by our body's current homeostasis?
-In studies of babies and rats saccharine (sweet) foods produced a similar positive facial expression whereas quinine (bitter) foods produced a negative expression -When sodium chloride suspension was introduction the reaction was dependent on sodium level in the body > those with high sodium were more likely to produce negative response > Indication of physiological state on motivation
What happens in the brain during the appetitive phase?
-In the APPETITIVE PHASE (before food is found) the dopaminergic system is activated and in the mesolimbic dopamine pathway one place where the dopamine is sent to is the amygdala (important in desiring food) -Destruction to this dopamine pathway causes animals to like but lose motivation to seek food > Dopamine is important for reward prediction/learning
What happens in the brain during the consummatory phase?
-In the CONSUMMATORY PHASE (once food is found) the nucleus accumbens is active which is involved in liking (opioid system allows us to enjoy food) -This terminates the appetitive phase and achieves satisfaction of a specific drive (reward rather than punishment)
What is binge eating?
-Included in the DSM-5 as it's own category and is characterised by recurring episodes of eating significantly more food in a short period than most people would -Results in lack of control, feelings of guilt/embarrassment/disgust and a rapid rise and fall of blood sugar which sends false messages to the brain craving food when the body doesn't need it
What biochemical abnormalities exist in bulimia nervosa?
-Increased ghrelin levels - lead to increased appetite which causes binges (returns to normal after therapy) -Low serotonin - blunted satiety due to excessive carb consumption
What happens to insulin and glucose levels in diabetes?
-Insulin levels remain constantly low and blood glucose is too high (unregulated) -People with diabetes eat more than normal because their cells are starving but they excrete most of their glucose rather than using it and lose weight
What is the role of ghrelin in eating?
-It is a peptide in the stomach that is released into the bloodstream when the stomach is empty -Activates NPY/AgRP containing neurons of arcuate nucleus (hypothalamus) to stimulate appetite -Too much ghrelin can lead to completely erratic and constant eating (induces feeling of hunger)
What is the role of the hypothalamus in eating?
-It is made up of a number of different nuclei talking to one another and reading signals about the body -The paraventricular nucleus (PVN) inhibits the lateral hypothalamus so is particularly important for satiety -Additional pathway from the PVN to the lateral hypothalamus which release neuropeptides (e.g. orexin) > leads to increase in persistence to seek food as well as increasing responses to incentive e.g. pleasant taste activates orexin receptors that override satiety (allows you to continue eating pleasant food) -Many axons containing dopamine pass through the lateral hypothesis which can alter taste sensation e.g. make food taste better when we are hungry
How is leptin important in the lipostatic hypothesis of eating?
-Leptin is the 'satiety' hormone which acts as long-term compensation for daily "mistakes" -It is released by body fat so when leptin is high we eat less, become more active and increase immune system activity (less need to conserve energy) -Body weight of adults is fairly constant and deviations from the set-point produce compensatory adjustments in eating
What do sham eating studies show?
-Look at the effect of removing the food from animals (rats eat, chew and swallow but food does not enter the stomach) -With familiar food rats start off eating normal amount but start eating more over time to try to achieve same feeling of fullness (learning) -With unfamiliar food eats more than usual to begin with so not relying on previous knowledge of nutritional content of the food
How does the Mexico vs Pima Indians study (Schulz et al, 2006) show how our genes and environment are linked?
-Looked at Arizona Pima Indians who had relocated to Mexico and others who remained in Arizona (both continued traditional farming) -Rates of type 2 diabetes varied dramatically: 38% in those who remained in Arizona but 6.9% those who relocated to Mexico > Genes make them more likely to conserve energy due to harsh southwestern desert (used to sparse diet) and when exposed to Western diet they would be more likely to develop diabetes (genetic predisposition)
What is the positive-incentive value of food for someone with anorexia?
-Many anorexics are actually obsessed with food, showing positive-incentive value for interacting with food is not the same as eating -Another incentive for anorexics is conditioning (associative learning) whereby aversive physiological effects of meals are enhanced in people that eat a little (strong negative association with eating and becoming fat) Therapy suggestion would be to introduce small portions
What are some of the factors affecting how much we eat?
-Package size -Variety available > humans given 10 different coloured M&Ms ate 43% more than the group given only 7 colours (Kahn & Wansink, 2004) -Multipacks -Size of bowl/utensiles -Environment (lighting, temperature, music) -Effort (shelled vs unshelled nuts) -Satiety signals > rely on learned knowledge to stop a meal and signals depend on volume and nutritional density of the food e.g. rats learn to prefer a flavour which provides the most calories (Myers et al, 2005)
What is the role of cholecystokinin (CCK) in eating?
-Peptide hormone present in some cells that line the intestines and some neurons that govern the gastrointestinal tract -Released in response to stimulation of the intestines by certain foods (e.g. fatty foods) and acts synergistically with gastric distension to inhibit feeding behaviour -CCK constricts the sphincter muscle (between stomach and duodenum) so the stomach holds more contents and fills more quickly = stomach distension (stimulates vagus nerve to send signals to hypothalamus)
How has bulimia nervosa been studied in rats?
-Research in rats has found that palatable foods are like addictive drugs and giving them 25% glucose solution (very sweet drink) for 12hrs followed by 12hrs fasting doubled their glucose intake from the drink in 10 days (highest after 20 days) > DA and opioid increased (produced appetite for palatable foods) > Rats showed addiction to big doses of sugar suggesting you can induce the cyclical behaviour of bulimia
How does gastric distension allow us to monitor food?
-Stomach wall has mechanosensory axons (monitor movement and respond to filling up) -Signals reach the brain via vagus nerve > medulla = inhibit feeding -Gastric bypasses cut into the stomach to make you fill full more easily
How is the reticular activating system implicated in arousal?
-Structure that extends from the medula to the forebrain which controls alertness and arousal -Acts as an attentional filter > if you lesion the RAS in cats it causes them to feel a coma but stimulating the area leads to hyperactivity (linked to ADHD in humans) -Important in increasing/decreasing arousal in cortical areas depending on the context
How can we explain individual differences in body weight?
-Weight of adopted children correlates more strongly with biological relatives than adoptive relatives > could be genetic or prenatal -In Prader-Willi syndrome (deletion of part of a chromosome) people have an insatiable appetite and eat pretty much anything they can get their hands on > 4/5 times higher ghrelin than average -Most cases of obesity relate to gene/environment interaction
What is the difference between anorectic and orexigenic peptides?
ANORECTIC peptides (e.g. MSH and CART) diminish appetite BUT when there is a decrease in leptin the responses mediated by these neurons are turned off and OREXIGENIC peptides (e.g. AgRP and NPY) are stimulated which activate the parasympathetic ANS and stimulate feeding behaviour
What does Yerkes-Dodson law (1908) argue about levels of arousal?
Levels of arousal can influence our performance depending on the nature of the task > higher arousal leads to increased performance on a simple task but only until optimum arousal levels are reached (consuming caffeine before taking part in a simple task would increase performance) On the other hand low levels of arousal increase performance on a complex task (again up to optimum arousal level)
Which study shows that social influences can affect satiety?
Redd & de Castro (1992) found a 60% increase in eating when with others ALTHOUGH the opposite effect is also possible e.g. eating less on a first date
What issues do lesions to the ventromedial hypothalamus cause?
The ventromedial and lateral hypothalamus work in opposition to each other so lesion to the ventromedial hypothalamus causes animals to overeat and become obese > Ventromedial hypothalamus is the satiety centre
Why are low and high calorie diets often ineffective?
Weight loss typically occurs within the initial period before a new settling point is reached (rate of weight loss slows) BUT lack of weight loss causes frustration and weight is quickly put back on at the end of the diet (rapid due to new metabolic rate with high incentive value of food)
What evidence is there for the role of gastric distension in inspiring motivation to eat?
When food is removed from a rat's stomach it will eat more to replace the missing contents = evidence of sensors in the stomach (Deutsch & Gonzalez, 1978)