hunger, eating + health

what is the cycle of hunger + eating due to

being a homeostatic mechanism → deviation from the optimum causes cravings/feelings of satiation to return the body to optimum

• this is the set-point assumption → hunger + eating works similar to a thermostat-regulated heating system

what are 9 organs in the gastrointestinal tract + how do they contribute to process of digestion

• mouth + salivary glands → masticate + produce saliva, which lubricates + contains amylase which begins to break down food

• oesophagus → transports food to stomach (set up for alkaline conditions, so acid reflux caused by drastic change in pH)

• stomach → churns + breaks down food by use of acid digestive enzymes e.g. hydrochloric acid + pepsin

• liver + gall bladder → adds further digestive enzymes into small intestine + bile to emulsify fats

• pancreas → produces insulin + glucagon to store + release energy

• small intestine → further digests food + absorbs nutrients

• large intestine → removes water + packs waste

• kidneys → filters out toxins for excretion

• rectum/anus + bladder → stores + expels waste

what are 2 key pancreatic hormones involved in digestion + what do they do

• insulin → converts carbohydrates e.g. glucose from the blood to storage as glycogen/proteins

• glucagon → converts stored glycogen + proteins to carbohydrates e.g. glucose to use as fuel when stores are low

for what reasons does our dietary intake need to be complex

• as we are omnivores → our diet includes a range of key elements that our bodies have evolved to process

• there is lots of variation of dietary intake between species → e.g. number of stomachs

• there is some variation of dietary intake within humans → e.g. dairy tolerance/allergies

what 4 core products does digestion produce + what storage mechanisms do they use

• lipids/fats → stored as fats (energy-efficient store)

• amino acids → stored as proteins in form of muscle tissue + neurotransmitters e.g. dopamine

• glucose → stored as glycogen in muscles + liver (fast-release)

• minerals/vitamins → stored in body structures e.g. bones/cells

why might some behavioural problems result from having an eating disorder

if someone isn’t getting sufficient amino acids from protein-rich foods, this may affect dopaminergic system due to lack of neurotransmitters → affects behavioural regulation

what 3 processes ensure eating needs are met

• homeostasis/set point theory

• hunger

• craving

due to what 2 factors can regulatory eating processes go wrong

• internal factors e.g. learning/emotions

• environmental factors e.g. toxic environment

what is the evolutionary + biological perspective of eating mechanism, and what are the two main mechanisms involved

our body has developed to be able to balance our intake + output through homeostasis

• homeostasis kicks in when our body’s set point is violated → e.g. if you are running out of energy, homeostasis provides signal that optimum must be reached again by inducing hunger

• metabolism → chemical changes by which energy is made available for organism’s use; cephalic + fasting phases occur when body is hungry or satiated

what is the ‘toxic environment’

the ease of accessibility of high-calorie food + drinks in modern Western civilisation

how are 3 different parts of our body utilised to detect whether we are running low on nutrients/fuel

• neurons in the hypothalamus are sensitive to shortage of glucose → hypothalamic regulatory nuclei

• the liver is sensitive to shortages of glucose + lipids

• the stomach sends the hormone ‘ghrelin’ to the brain if unstimulated + needing food

what factor can account for genetic aspect of eating behaviour

gene variation can cause over or under-release of the ghrelin hormone, associated with over + under-eating

what does set-point theory predict occurs when the body is low on fuel

we experience both:

• hunger → a motivational state, due to low levels of fatty acids/glucose

• craving → an automatic behavioural/psychological state

the body corrects this by releasing glucagon to convert glycogen energy stores into glucose + taking in more food

what 4 signals in the body indicate satiety

• adequate glucose + lipid levels detected in the brain + liver

• stomach distension

• behavioural signals e.g. high buccal activity (lots of chewing)

• psychological signals e.g. high levels of sensory stimulation (taste + smell)

what external stimuli can produce feelings of satiety in the body

appetite-suppressant chemicals e.g. caffeine + amphetamines

• means drinks with high levels of caffeine don’t provide much energy in actuality, but trick the brain by acting on dopaminergic system

what did previous research suggest was the part of the body responsible for satiety

proposed there was a ‘centre’ in the brain (within the hypothalamus) that dictated satiety by detecting that glucose levels were back to normal

how does more recent research propose the body reaches satiety (what 3 are involved)

proposes there is no one ‘centre’ but rather the process is more hormonally-controlled → by ghrelin, neuropeptide Y + serotonin

what hormone do fat tissues secrete + what effects does it have on satiety

if too much energy is going into fat tissues, leptin is released → has 2 main effects:

• increases the body’s metabolic rate, meaning energy is expended faster

• decreases food intake by desensitising the brain to hunger signals + inhibiting the effect of other hormones that drive eating, e.g. neuropeptide Y

what is the satiety cascade + what are its 4 stages

the stages in which the body registers that it has consumed enough. includes:

• sensory → high stimulation

• cognitive signals

• post-ingestive → blood glucose rates increasing

• post-absorptive → hormones e.g. leptin being released

what are the health complications with normative poor eating

causes poor nutrition + problems with the brain/body

what method was used in the Minnesota starvation experiment (Keys et al., 1950)

unethical experiment which studied the cognitive, social + emotional effects of starvation in 35 men who were coerced into either taking part or joining the army

• men had to walk 22 miles a week, with the goal of losing 25% of their bodyweight

• were afterwards given 3 months of rehabilitation in order to gain weight back

what were the 4 broad effects of starvation on participants in the Minnesota starvation experiment (1950)

• physical effects → extremities formed extra fluid, sex drive decreased, hair fell out and coordination/balance was lost

• cognitive effects → eating became ritualised + compulsive, and concentration decreased

• social + emotional instability → relates to the tryptophan cycle (precursor to serotonin; emotional consequences if it isn’t ingested)

• stunted physical + mental development

starvation effects also seen in anorexia nervosa have been based on these studies

what occurred in the rehabilitation stage of the Minnesota starvation experiment (1950)

over the course of 3 months, some participants initially dropped in weight even though food intake was increasing

• some participants took 2 years to recover previous weight

• men were generally found to weigh more + have more fat stores than before the experiment

what 3 nutritional deficits are associated with starvation

• scurvy

• rickets

• Korsakoff’s amnesia → memory disorder caused by vitamin B1 deficiency

can starvation effects cross generations

yes → parents can pass on problematic + compensatory eating behaviours to their children, e.g. obesity observed in children of previously-starved mothers

what are health implications of obesity

linked to premature mortality, which can be contributed to by:

• hypertension

• type 2 diabetes

• dyslipidemia

• increased cancer risk

• liver disease

• reproductive + mood disorders

• cardiovascular disease + hypertension

what specific problems is obesity linked to in children

can cause increase in experiences of bullying + school absence, which may contribute to experience of stigma + issues with self-esteem

what are 4 factors that draw us away from homeostasis

• genetics → gene associated with leptin signaling may cause predisposition to preferring sweet/calorific foods

• learned taste preferences + aversions

• social learning + pressures → from family/peers

• food industry producing high increase of calorific food → creates toxic environment

how does genetics incluence what foods we are likely to eat

genetic factors make us more likely to eat particular foods → other more ‘grown-up’ tastes (e.g. olives, acidic foods) are usually learned later

• we are predisposed to enjoying high-energy + taste foods (ones that are sweet, salty + fatty) due to more likely containing nutrients

• we are less likely to enjoy bitter foods due to their association with toxicity

what 4 factors are learned taste preferences + aversions influenced by

• culture → foods common in one’s own culture are likely to be preferred

• upbringing → foods experienced early in one’s upbringing tend to be more readily approached

• conditioned taste aversions → powerful classical conditioning paradigm in which food associated with negative experience (e.g. being ill) makes you feel sick again in the future

• satiety to specific foods, e.g. dye to having eaten it recently → keeps our diet varied

what is sensory-specific satiety + what is an associated experimental finding

refers to the decrease in pleasantness + consumption of a specific food after eating it to satiety

• lab experiment found that being given food of different flavours/shapes (altering sensory properties) increased both food intake + ratings of pleasantness from participants

how does social learning change what we eat

social/observational learning influences us to eat in a number of ways influenced the people surrounding us. influences:

• types of foods

• speed of eating

• amount eaten

this acts as a powerful cultural influence, as people adopt eating patterns that are considered normal/customary

what are 5 environmental factors that contribute to how much one eats

• lighting → we tend to eat more in dim lighting

• temperature → we tend to eat more when cold rather than hot

• portion sizes → varying the size of the plate changes perception of how much one is eating

• smell → both of food + environment itself

• location/proximity of foods

what is the Malthusian hypothesis + how does it relate to the food industry

the rate of population increases linearly, so production of food also needs to be boosted → agriculture + food industry therefore ensures we do not starve due to an increasing population

why is the food industry currently regarded as a toxic place

• currently sells processed, fatty + sugary foods in large quantities for relatively cheap → ensures profit margins

• premium prices are placed on more ‘healthy’ foods which are often out of season

what is an example of the toxicity of the food industry

high fructose corn syrup (HFCS) → created due to overproduction of corn in 1970s US; was supplied cheaply for use in many different products

how is HFCS related to the toxicity of the food industry

its production + consumption has been directly related to obesity levels → has caused unwanted side effects e.g. fatty liver, decreased insulin sensitivity + gout precursors

what was the aim + method of Spurlock (2004)’s ‘super size me’ documentary

aimed to draw attention to the fact that the only meal options available in fast food outlets e.g. McDonalds were high-calorie

• tested what the negative effects of eating 3 ‘super-size’ meals a day was on health were

what effects did Spurlock (2004) find + what was a limitation of this study

in 30 days he gained 11kg, had far above-average cholesterol, mood swings + liver problems → resulted in significant negative publicity for fast-food outlets, portion sizes changed + healthier options e.g. salads/wraps were introduced

• limitation of the study was that it was subsequently revealed Spurlock had a significant alcohol problem → may have contributed to the liver function issues

what is Brownell’s ‘toxic environment’

describes the way in which human evolution + the modern Western environment are completely at odds → in our current environment, we can access as much food as we want, which happens to be highly processed due to the food industry

in what 2 ways does the ‘toxic environment’ relate to culture

• in cultures where food is scarce, obesity is valued as a status symbol

• in cultures where food is plentiful (e.g. in the current West), obesity is stigmatised as a sign of weakness

how does the ‘toxic environment’ theory propose that the way humans evolved impacts how we eat

points out that we evolved as hunter-gatherers → when food was scarce, homeostatic mechanisms benefited us by slowly releasing stored glucose/fats for energy

• our genes mean give us a disposition to eat as much as we can when we can, so that we can live off of fat stores in leaner times

• in evolution, high-energy food was only seasonally available → means high salt + sugar foods are often preferred

how does the ‘toxic environment’ theory propose the food we have accessible has changed in the past 60 years

the foods we are genetically-programmed to prefer eating are now in abundance → the food industry often packs as much sugar + salt into foods as possible to make them cheaper + more palatable

• means more ‘liquid calories’ are accessible while healthier foods become more expensive + harder to obtain

how else does toxic environment theory propose culture has changed in recent years + how does this contribute to poor health/eating habits

exercise has generally decreased in the population, and more time is spent on screens, including viewing adverts for food + drinks

• increased screen-time associated with dissociative effects → reduces self-control, including in regard to what we eat

• less activity than previously → body is more likely to become inflamed due to needing to pass the nutrients it has stored → inflammation associated with depression

how has giving cooking lessons to people with PTSD helped to alleviate symptoms

has resulted in patients having a better diet → this reduces inflammation, which brings better psychological outcomes + a bettering of symptoms