Please enable JavaScript.
Coggle requires JavaScript to display documents.
Biopsych - Motivation and Eating (Y2) - Coggle Diagram
Biopsych - Motivation and Eating (Y2)
Major motivation theories
Motivation explained
Motivation is what initiates, directs and maintains our behaviours
No single theory accounts for all aspects of motivation - each contributes an important perspective
Questions -
-> Is motivation innate or learnt?
-> What is it that motivates our behaviour?
-> How do biological, social, cognitive and emotional factors influence our motivation?
Urge to behave or act in a way that satisfies conditions, wishes, desires or goals
Motivation rooted in basic impulse to optimise wellbeing, minimise physical pain and maximise pleasure
Instinct theories - Behaviour is motivated by instinct that is innate and activated by environmental stimuli
Early theory - suggests that instincts explain all human behaviours and that these are unlearned, innate and automatic
McDougall (1908) proposed 18 different instincts e.g. curiosity, sex, hunger
Causes us to respond in a specific way to a particular stimuli
Trigger behaviours that aid in survival
In humans, many reflexes are examples of instinctive behaviours e.g. suckling reflex
But - instincts cannot explain all behaviours and are difficult to detect
Maslow's hierarchy of needs - different motives compete, with basic survival needs being satisfied first before we can satisfy higher level needs
Hierarchy likely not linear
Research shows that only the two lowest needs are hierarchial
Humans are motivated at any one time by a complex array of needs
Limitations - hard to test and culturally specific
Defines motivation as the process of satisfying certain needs that are required for long-term survival and development
Some needs are basic to all, and in their absence nothing else matters - as needs are satisfied, we move up the hierarchy into new motivators
Physiological and actualisation needs - higher order only motivates when lower order is met
A need is a relatively lasting condition or feeling that requires relief or satisfaction, and tends to influence action over the long term
Some needs (like hunger) may decrease when satisfied, while others (like curiosity) may not
Basic physiological needs -> safety needs -> belonging needs -> self esteem needs -> self actualisation
Optimal arousal theory - behaviour is motivated by the need to achieve optimum levels of arousal
Aim of motivation is to maintain an optimum level of arousal (=state of alertness/readiness, mental or physical activation)
Behaviour is a response to a need to raise or lower arousal levels
If you need to raise your arousal levels, you are motivated to do so
If you need to lower arousal levels, you are motivated to do so
Individual differences in the 'optimal' arousal level - some people require constant stimulation to maintain an optimal arousal level
Yerkes-Dodson Law (1908) - levels of arousal influence performance -
-> Increased arousal can help improve performance, but only up to a certain point, after which it diminishes
-> Complex tasks are affected more by non-optimal levels of arousal
Two primary arousal systems -
-> Autonomic nervous system - arouses body
-> Cortical arousal system - arouses brain
Expands on drive reduction theory by considering arousal as motivation
Dopamine is main motivator in body
Motivation is linked to biological factors that control reward sensitivity and goal-driven behaviour
Reward system in the human body spurs physiological arousal, which motivates individuals to engage in whatever behaviour is necessary to relieve their arousal
Optimal levels for peak performance - when too low or too high, performance suffers
Traits like impulsivity and sensation seeking predispose people to engage in activities they find physiologically arousing
Reward system - arousal theory proposes motivation is strongly liked to reward sensitivity and goal-driven behaviour
Mesolimbic dopamine system - influences motivation for certain-goal driven behaviours that will elicit a reward or satisfy a craving
Encourages engagement in whatever behavior is necessary to satisfy or relieve arousal
E.g. if substance abuse activates this, you may be more motivated to consume them
Electrical self stimulation as a method of measuring this - Milner and Olds, 1950s - motivated to perform behaviours that give a reward or are reinforced by a reward
Drive reduction theoryy - motivation originates from biological needs to maintain the body in a state of balance
Incentive theory - behaviour is motivated by internal (intrinsic) and external (extrinsic) incentives or rewards
Motivations are separated into drives (biological) and motives (social and psychological)
Motivations can be intrinsic or extrinsic
Our motivations are usually a mixture of both of these, and their influence changes over time
Motivation can be stimulated by uncomfortable or aversive conditions, or by attractions - we also become motivated when deprived of a stimulus
Motivation v emotion -
Motivation is the wants or needs that direct behaviour
Emotions are subjective states of being that we often describe as a feeling
Both influence behaviour and can lead to action, and emotion can be a motivator
Intrinsic and extrinsic motivation -
Intrinsically-motivated behaviours are generated by sense of personal satisfaction - driven by interest and enjoyment
-> Critical in cognitive, social and physical development - people perform better and improve skills when they care
-> Autonomy, mastery and purpose
Extrinsically-motivated behaviours are performed in order to receive rewards from others
-> Compensation, punishment and reward
The two interact and change in their importance
-> Sometimes, intrinsic motivation can diminish when extrinsic motivation is given - overjustification effect
-> Can lead to extinguishing intrinsic motivation and creating a dependence on extrinsic rewards for continued performance
Drive reduction theory
Physiological needs create drives which motivates us to satisfy them (drive reduction) - Hull, 1951:
This allows for homeostasis - the maintenance of a steady internal state
Our survival depends on our ability to maintain these internal states within narrowly defined ranges, despite being subject to constantly changing external forces
Relation to eating behaviour - Energy storage in the body
Carbohydrates, fats and proteins are the major constituents of foods and serve as fuel molecules for the human body
These are absorbed into the bloodstream and used by cells
Energy is stored in the body in 3 forms -
-> Fat - preferred form of storage
-> Glycogen -> made and stored primarily in liver and muscle, used to maintain blood sugar levels
-> Protein - broken down and used for energy when other stores are depleted
Homeostasis -
Control centre receives input from receptors, and directs effectors based on this to correct imbalance detected by the control centre
Biological drives correct disturbances of homeostasis - unsatisfied drives are detected by neurons concentrated in the hypothalamus of the brain
Body automatically responds to survival drives, and you become motivated to correct these disturbances
One way the body increases this behavioural motivation is through arousal
What creates the drive
According to Glucostatic hypothesis - it is the need to maintain glucose and glycogen levels
A drop in these causes increased appetite and triggers eating
Mechanism -
-> During / after a meal, insulin levels increase
-> Insulin allows cells to make use of glucose
-> Promotes storage of excess glucose as glycogen
Insulin -
-> Produced by the pancreas
-> it can enter the brain and acts to reduce appetite
-> Later, as insulin levels decline, hunger returns
-> So, insulin is one of the hormones that controls appetite
The physiological aim of the drive is homeostasis
Appetite hormones - timing - after a meal - rise of glucose levels in blood, rise of insulin levels, fall in ghrelin levels and no effect on leptin
Body weight remains relatively constant -
Lipostatic hypothesis; level of body fat influences regulation of food consumption to maintain a stable body weight
Signal - Leptin (produced by fat cells) suppresses appetite
-> Leptin is produced by fat (adipose tissues), stomach and other organs
-> Leptin levels are positively correlated with the amount of body fat mass
-> Leptin secretion is not influenced by meal patterns
-> Levels follow a daily rhythm peaking between midnight and early morning
Ghrelin (appetite stimulant) is also influenced by body fat levels, being low in obese subjects, higher in lean subjects and markedly elevated in anorexia
-> Peptide hormone made by the stomach
-> Influenced by body fat levels
-> However, increases between meals and falls after food is consumed
-> Intravenous infusion of Ghrelin causes more food to be consumed
-> Ghrelin - appetite stimulant - signals to hypothalamus about hunger
What is the regulator - Hypothalamus performs a variety of regulatory functions
It is responsible for the regulation of the autonomic nervous system including metabolic processes
Hypothalamus contains receptors for many peptide hormones (including Ghrelin, Insulin, Leptin)
Regulator for appetite and feeding behaviours -
-> Removal of rat lateral hypothalamus causes diminished appetite for food (Hetherington and Ranson, 1940)
-> Electrical stimulation of lateral hypothalamus causes rat to feed, even when well fed
Lateral hypothalamus -> hunger centre
Lesion to ventromedial hypothalamus causes animals to overeat and become obese - satiety centre
Elliot Stellar (1954) - dual centre model for feeding - balance of activity between lateral (hunger) and ventromedial hypothalamus (satiety) controls eating
Lateral hypothalamus - lesions also cause:
-> Wide range of severe motor disturbances
-> General lack of responsiveness to sensory input (not only food and drink)
-> Likely damage to nearby fibres of passage important for sensory and reward processing
-> More general role in motivation
Despite this, hypothalamus is an important control centre for feeding and metabolism:
It receives sensory information from the stomach / intestines
It is sensitive to leptin/ghrelin/insulin and other hormones
It can regulate metabolism via the autonomic nervous system
It outputs to nucleus accumbens, orbitofrontal cortex (OFC)
Hypothalamus seems to act as a thermostat, regulating hunger and metabolism (energy usage)
Hypothalamus and satiety:
Arcuate nucleus of the hypothalamus influences metabolism - centre of neural networks that interact with receptors in the blood and guts
Certain neurons in the paraventricular neurons of the hypothalamus have been shown to act as nutrient sensors that influence feeding and satiety
Serotonin produced satiety -
Reduces amount of food consumed in each meal, causing resistance to palatable foods and associated with a move away from fatty foods - could be used to combat obesity
Set point theory -
If we fall below ideal weight (Set point) our body will increase hunger and decrease energy expenditure
Basic metabolic rate (BMR) - the rate your body burns calories at rest
If we go above our set point, the hypothalamus tells us to stop eating and raises our metabolic rate to burn any excess food
Set point likely relates to component of our body composition rather than body weight, such as % fat (lipostatic theory)
Evidence - despite daily variation in energy intake and expenditure, most adults maintain a relatively stable body weight, with variance only around 0.5% over periods of 6-10 weeks
Set point v settling point -
Set point theory = oversimplified - settling point aims to explain how body weight varies around a set point
There are other factors which can influence body weight and body composition
From the late 1970s, the percentage of overweight individuals started to rise
Setpoint is not fixed - it is influenced by societal factors (e.g. overabundance and easy availability of food, sedentary lifestyles and labour saving technologies)
Also, people can lower setpoint through dietary / exercise changes - settling point is where the body will reset its set point too when a long term change in diet occurs
In settling point model, negative feedback leads to limits in further changes, where is in the set point model, any change will lead to a reset to this point
Interaction of biological / environmental factors = dynamic equilibrium, or a settling point
Why do some people gain weight and others do not?
Differences in energy expenditure - non exercise activity thermogenesis, basal metabolic rate and diet-induced thermogenesis
Differences in gut microbiome compositions
Genetic and epigenetic factors - around 100 humans chromosome loci linked to it - affect gut microbiome
Why do weight loss programs not work?
Because of settling points - when normal conditions are restored, you return to your natural weight point - permanent lifestyle change is the only way to continuously remain at a smaller weight
Primary drives are innate biological needs, whereas secondary drives are associated with or indirectly satisfy primary drives
Drives are thought to underlie all behaviour, in that behaviours are only conditioned, or learned, if they satisfy a drive
Drive-reduction theory has been criticised for failing to explain how secondary reinforcers reduce drive or why individuals engage in pleasure-seeking behaviours
When a physiological need is not satisfied, a negative state of tension is created; when the need is satisfied, drive is reduced
Drives are instinctual needs that can motivate behaviour
Role of habits - once a behaviour is shown to successfully reduce a drive, we are more likely to engage in that behaviour again when faced with the same drive again (Graham and Weiner, 1996)
Multiple drives can lead to rapid learning compared to single drives
Critiques -
Validity - cannot explain why tension is voluntarily increased by exploring their environments
Complications of pleasure seeking behaviours - seeking more stimulation despite being relaxed and fulfilled
Summary -
Drive reduction theory tells us that we are motivated to act in a certain way because of a physiological need to maintain homeostasis
Hormones that stimulate or suppress appetite are key mechanisms
Hypothalamus is sensitive to these signals and acts to regulate our eating behaviour and metabolic rate to maintain stable body weight (set point)
But other factors also important - settling point
Digestion processes - gut microbiome
Steps in digestion -
Chewing breaks up food, mixing it with saliva
Saliva lubricates food and begins its digestion
Swallowing moves food and drink down the oesophagus to the stomach
Primary function of stomach - storage reservoir - HCl acid in the stomch breaks food into small particles, and pepsin starts process of breaking down proteins into amino acids
Stomach empties its contents through the pyloric sphincter into the duodenum, the upper portion of the intestine, where most of the absorption occurs
Digestive enzymes in this area from gallbladder and pancreas break proteins into amino acids, and starch and complex sugar to simple sugar - simple sugars and amino acids readily pass through the duodenum wall into the bloodstream and to the liver
Fats are emulsified by bile, manufactured in the liver and stored in the gallbladder until it is released into the duodenum - emulsified fat cannot pass through the wall and is carried by small ducts to the lymphatic system
Most of the remaining water and electrolytes are absorbed from the waste in the large intestine, and the remainder is ejected from the anus
Fat as main method of storage - stores double the amount of energy per gram than glycogen, and holds less water than glycogen also
Three phases of energy metabolism -
Cephalic phase - Preparatory phase beginning with the sight, smell or thought of food, ending with the food being absorbed into the bloodstream
Absorptive phase - Energy absorbed into bloodstream, which meets the body’s immediate needs
Fasting phase - Period during which all of the unstored energy from the previous meal has been used and the body is withdrawing energy from its reserves to meet immediate energy requirements - ends with cephalic phase starting again
Rapid weight gain usually happens when the fasting phase is skipped
Insulin and glucagon are vital hormones in this process
Insulin promotes glucose use as primary energy source, promotes the conversion of bloodborne fuels to storable forms (glucose to glycogen, fats to proteins) and promotes the storage of glycogen in the liver and muscle, fat in adipose tissue and proteins in muscle
-> In cephalic phase, it aims to lower the levels of bloodborne fuels
-> Absorptive phase aims to minimise fuels by storing them better
Glucagon in fasting phase -> converts protein and glycogen to glucose
Role of the gastrointestinal tract in satiety:
Cannon and Washburn (1912) - stomach contractions are the feeling of hunger when you have an empty stomach
Gastrointestinal tract is implicated in satiety
Ingested food interacts with receptors in the gastrointestinal tract and this causes peptides to be released - circulating gut peptides inform the brain about quantity and nature of food, and this has a role in satiety (insulin, glucagon)
Satiety peptides are those which bind to sites on the hypothalamus involved in metabolism
Hunger peptides are also synthesised in the hypothalamus and produce metabolic effects to increase eating (neuropeptide Y, orexin-A and ghrelin)
Positive incentive theory and mesocorticolimbic system
Positive incentive theory -
This theory states that we are motivated to eat not by internal energy deficits, but by the anticipated pleasure of eating -> positive incentive value
It also emphasises the role of external stimuli such as the time of day, the sight and smell of food and the social context
Incentives - how much we eat:
Evidence shows our consumption is influenced by a range of factors
-> Package size (Wansink, 2004)
-> Size of bowl / utensils (Wansink et al, 2003)
-> Environment (lighting, Sommer, 1969; temperature; soft music, Caldwell and Friedman, 1974)
-> Effort (shelled v unshelled nuts; Schacter and Friedman, 1974
-> Social influences - 60% increase in eating when we are with others (Redd and de Castro, 1992) - can also cause opposite effect
Rats increased their calorie intake by 84% and their weight by 49% when they have a variety of foods to choose from (Rogers and Blundell, 1980)
Sensory specific satiety (SSS) - decrease in the pleasantness / consumption of a specific food after eating it due to satiety - still room for desert
As you eat one food, the positive incentive value for all food declines slightly, but for that food declines strongly
Orbitofrontal cortex -
Cell recordings show populations of neurons here respond to particular tastes (Rolls et al, 1989, 1990)
Brain activity also reflects incentive value of a particular food
Activity of taste neurons for a food with which a monkey is fed to satiety - decrease to zero - SSS
Underlying neurobiology of PIT - Bassareo, 1999
Activation of mesolimbic dopamine pathway = key reward circuit
Projects from ventral tegmental areas (VTA) to regions including - nucleus accumbens and frontal cortex
Feeding has been shown to trigger dopamine release in nucleus accumbens
Eating = rewarding
The Chocolate Craving Study (Rolls and McCabe, 2007) -
-> MRI study - Chocolate pictures = activation in OFC and nucleus accumbens
-> Larger effects in cravers v non-cravers of chocolate
-> Good evidence that reward system activation reflects the positive incentive value of food
Incentive theory argues behaviour is primarily extrinsically motivated - people are more motivated to perform activities if they receive a reward afterwards, rather than simply because they enjoy the activities themselves
Intrinsic behaviours are performed because of personal satisfaction
-> Decreases over time if extrinsic motivators vary depending on factors such as self esteem
Extrinsic behaviours are performed to receive something from others
-> Efficacy of these depends on factors such as self-esteem, locus of control, self-efficacy and neuroticism
-> They tend to be used to motivate interest in an activity that is useful but someone has no interest in
Do we eat at certain times of the day or in certain situations out of habit, or cultural norms?
Can external stimuli trigger eating?
Eating is able to conditioned - Weingarten, 1983
-> Classical conditioning of eating in rats
-> Even when well-fed, eating was triggered by an external stimulus previously associated with food
-> Consistent with the positive incentive theory, but not drive reduction theory
The Buffet Effect: Rolls, Rolls and Rowe (1982)
Variety of food on offer - more sandwiches are consumed when they were offered with multiple filings, more pasta consumed if there is a variety of pasta shapes
This is consistent with positive incentive theory, but not drive reduction - we eat for pleasure and stimuli, instead of being motivated by drive
Summary - positive-incentive theory states that motivation to eat is driven by anticipated reward value of food and environmental factors
Can explain many findings better than drive reduction
Dopamine reward system is activated by food
Mesocortical dopamine projects to orbitofrontal cortex (OFC)
OFC neurons respond to specific tastes - activity reduces when SSS occurs
Eating disorders
Anorexia nervosa - persistent restriction of energy intake leading to significantly low body weight
Intense fear of gaining weight, or persistent behaviour that interferes with weight gain
Disturbance in experience of own body weight, lack of recognition of seriousness of current low body weight
Biological explanations -
Hypothalamus dysfunction theory - Garfinkel and Gardner (1982)
Disturbed hypothalamic function means lack of weight thermostat
Other impaired hypothalamic functions support this (e.g. body temperature control)
BMI correlated with GM in the hypothalamus
Other regions atrophied also
Dopamine (Bailer, 2012)
Some studies suggest the dopamine system might be hypersensitive in anorexia
Amphetamine (which activates dopamine system) leads to anxiety in anorexia nervosa, but euphoria in healthy controls
Could explain why dopamine released by food produces anxiety (not pleasure) in anorexia
However - are these findings cause and effect or mal/under nutrition?
Other factors are clearly important, such as trauma, unhealthy parental attitudes, personality traits and stress - genetic, psychological and sociocultural influences
Changes in prevalence from last 20 years point to sociocultural influences e.g. media promoting unhealthy body ideals
Bulimia -
Recurrent episodes of binge eating and eating more than most in a discrete time period
A sense of lack of control over eating
Compensatory behaviour to prevent weight gain - vomiting, laxatives, fasting, excessive exercise
Biological explanations - Ely, 2017 -
Binge eating, loss of control and eating despite fullness
In striatum and amygdala, brain activity towards food not reduced when full v hungry
Suggests disinhibited eating in BN could result in failure to devalue food reward when full up
Example of binge eating - Prader-Willi Syndrome -
Genetic disorder - insatiable hunger is a behavioural phenotype
Genetic cause - paternal deletion of chromosome 15
-> Disrupts development and functioning of hypothalamus and several neurotransmitters involved in eating (Dimitropoulos et al, 2000)
Symptoms -
-> Insatiable hunger
-> Slow metabolism
-> Other physical and neurological symptoms - muscle weakness, small hands and feet, stubbornness, feeding difficulties in infancy, tantrums and compulsivity
Untreated - most people become extremely obese and die in early adulthood
Final summary - in eating behaviours -
Drive reduction theories emphasise importance of maintaining homeostasis -> hypothalamus
Incentive theories emphasises reward value of food -> dopamine system
Eating disorders linked to both hypothalamus and dopamine abnormalities, but other factors are important
Obesity
Positive incentive theory -
Motivation to eat is driven by anticipated reward value of food and environmental factors
Can explain findings better than drive reduction
Dopamine rewards are activated by food - mesocortical dopamine projects to OFC
OFC neurons respond to specific tastes - activity reduces when sensory-specific satiety occurs
Importance of these factors show our set point is not fixed or stable
Instead, cultural factors such as food availability, packaging and advertising are major influences
These fit with positive incentive theories which emphasise anticipated pleasure of eating and how external stimuli motivate certain eating patterns
Health risks - diabetes, cardiovascular disease and others, and complications related to it account for 10% of national health care
Drive theory - set point is not well-identified
Role of leptin
-> Lower sensitivity to this in hypothalamus results in no reduction in urge to eat
-> However, studies find no differences in Leptin sensitivity between obese and non-obese individuals
In some cases, obesity can be triggered by mutations in the LEP gene which provided leptin instructions
-> Leptin released to maintain stability in body fat %
-> Leptin i a satiety hormone that reduces appetite by binding to hypothalamic receptors
-> Defective gene can cause inadequate leptin production
-> Hypothalamus under-assesses body fat stores, increasing urge to eat
-> Congenital leptin deficiency is a condition that causes extreme hunger, chronic excessive eating and severe obestiy
A global epidemic - drive reduction can explain the increased weight of the population:
Other factors in obesity - metabolic differences, quantity and sensitivity to hormones, eating patterns, food packaging, food availability, physical inactivity, eating environment and body image
Genetics - families share eating and exercise habits, and the largest transmissable variation is cultural
Changes in culture - lifestyles have become more sedentary, leading to higher risk of obesity
Positive incentive theories - eating later; more fast food and social eating has changed when we eat and made us more likely to eat out and having more preserved food
-> Fatty foods lead to more pleasure and positive incentive to consume that food
Fast food - availability is higher than ever, packaged, convenient, heavily advertised, attractive, cheaper, added sugar /high in fat
-> Positive incentive value
-> higher energy density, greater saturated fat, reduced complex carbohydrates and fibre, reduced fruit and vegetables
Physical inactivity - energy use has decreased but energy intake has increased
Treatment of over-eating and high body-fat levels:
Serotonergic agonists - impact short-term satiety signals involved with meal consumption
Gastric surgery - reduces absorption, leads to weight loss