PSAY3 Revision

• Mills et al (1998): 207 male inmates - Canada - aggression measured on reported of committing serious miscounduct compared to score on alcohol dependancy scale: those with substantial alcohol dependancy = likely to commit more serious crime; SUPPORTS importation model: charcteristics (alcohol) brought into the institution. 
• Kane & Janus (1981): non-whites, younger inmates = more likely to be more aggressive in prison; SUPPORTS importation model: shows charcteristics (race/age) brought into institution. 
• Zimbardo (2007): emphasies that the situation an individual is in = powerful influence on their willingness to harm others/ Stanford prison experient found that institutional factors like external constraints/peer pressure led to aggression; SUPPORTS the deprivation model and lucifer effect as it shows that situational factors increase aggression however CONTRADICTS the importation model; shows that nurture/social factors also affect aggression. 

• Institutional aggression = aggression that takes place as a result of being in an insituttional setting (prison/hosipial). 
• Includes aggression within a group (different prisoners) or between different groups (prisoners and guards).
• Importation Model: Irwin & Cressey (1962): prisoners bring existing aggressive personalities into insitution and continue to behave the same way; NOT caused by situation: e.g. gang members co tinue gang culture in prison leading to a high number of violent attacks. Aggression is influenced by education/employment histore/race. 
• The Lucifer Effect: Zimbardo: situational factors increase aggression: e.g change in power status within the insitution. 
• The Deprivation Model: Sykes: deprivation of liberty (respect/civil rights), deprivation of autonomy (no choices), deprivation of security (scared of other inmates) cause aggression to reduce stress. 

• APPLICATIONS: if alcohol dependancy = aggression can be dealt with/overcrowding also can be dealt with (however its found that increasing personal space has no effect) also not COST EFFECTIVE. 
• LOW POPULATION: most studies conducted in prison. 
• SENSITIVE ISSUE: aggression = anti-social behaviour; when researching, participants may not behave as aggressive as they would do when being observed. 
• CULTURAL BIAS: no specific operationalised count for aggression, definition of aggression varies from one cultural group to another. 
• DETERMINISTIC: aggession caused by situational factors; the deprivation model/lucifer effect IGNORES FREE WILL but can't be an excuse for acting aggressively. 
• REDUCTIONIST: the deprivation model ignores biological factors like genes/hormones however its been proven that testosterone increases aggression.

• Raine Et Al (1997): compared PET scans of 41 murderers (39 m, 2 f) and non murderers whilst doing visual task: murderers = less activity in prefrontal cortex/amygdala; SUPPORTS that prefrontal cortex is not used; cant control inappropriate display of aggression.
• Lewis (1986): 15 murderers (13 m, 2 f) on death row: medical records/family interviews/neurological tests = inmates had experienced severe brain injury (usually during childhood); SUPPORTS that brain damage can affect the control of innapropriate display of aggression. 
• Charles Whitman (1966): shot 12 people, post mortem = tumour pressing on his limbic system; SUPPORTS that the limbic system affects aggression. 
• Wagner Et Al (1979): male mouse castrated = reduction in testosterone = less aggression, if the mouse was given tesotserone = aggression increased; SUPPORTS that testosterone is an important hormone in aggression. 
• Davidson, Putnam & Larson (2000): lower levels of serotonin in violent criminals; SUPPORTS that neurotransmitters serotonin keeps aggressive social response in check. 
• Harrison Et Al: gave participants testosterone and computer game aimed to frustrate; aggression varied; shows that testosterone is only a contributing factors
  

NEURAL:

• Structures in brain: limbic system = responsible for insticintive behaviour (eating/aggression/sexual activity) linked to aggression. 
• The hypathalamus/amygdala (in medial temporal lobe)  = makes people act aggressively. 
• Prefrontal cortex = controls inappropriate display of aggression; any damage to it will make it harder to control our aggressive insticts. 
• Neurotransmitters (chemicals that send messages from 1 area of the brain to another): serotonin, dopamine, noradrenaline. Serotonin = role in emotions like impislive aggression during social decision making. Impulsive aggression = responding with aggression when faced with frustration; serotonin keeps aggressive social response in check. 

HORMONAL: 

• Testosterone = androgen produced in male testes/adrenal cortex - it influences aggression as it affects bits of the brain like the amygdala. 
• An adult male makes 10 times more testosterone than a female; men are usually more aggressive. 

• APPLICATIONS: if aggressive due to imbalance of neurotransmitters; could be treated by giving serotonin increasing drugs; has been succesful in aggressive demential patients.
• SUPPORT: direct stimulation of amygdala in hamsters = aggression, also amygdala is more active when under threat. 
• REDUCTIONIST: hard to isolate precise areas of brain; oversimplified, the compelex interconnectedness of brain, simlarly they argue that neurotransmitters could account for aggressive behaviour as they're part of a wider network. 
• DETERMINSTIC: biological approach says aggresison is innate; FREE WILL IS IGNORED. Watching footbal, fans testoserone levels increase; SHOULDN'T IGNORE ENVIORNMENTAL factors as they also affect aggression.  
• NO CAUSE & EFFECT: there's a lot of correlation studies however perhaps testosterone increases due to aggression not the other way around. 

• Siffre (1975): 179 days in cave - Texas, no external zeitgebers, sleep wake cycle = 25-32 hours, body temperature = 25 hours. SUPPORTS that absence of natural light-dark cycle; body clock can regulate circadian rhythm but not accurately. 
• Aschoff & Wever: students in underground bunker, no light cues, sleep wake cycle = 24-27 hours; SUPPORTS that endogenous pacemakers can control the sleep wake cycle. 
• Ralphe & Menake (1990): mutant hamster with 20 hour sleep wake cycle, SCN transplant with a 24 hour hamster, hamster adopted the donors sleep wake cycle. SCN was destroyed, circadian cycles = random; SUPPORTING that the SCN is the main endogenous pacemaker. 
• Lews & Lobban (1950's): participants in Arctic circle, unknowingly had their watches set to 21/27 hours. Constant light; no exogenous zeitgebers (light-dark cycle); participants sleep wake cycle operated to their watches; SHOWING that zeitgebers can override the natural 24 hour circadian biological clock. 
• Folkard Et Al: gradually reduced circadian rhythm with a quickening clock, but at 22 hours, participants own rhythms took over again; CONTRADICTS Lewis & Lobban as it shows that endogenous pacemakers cant be completely overriden by external zeitgebers. 
• Pinel (1999): 70% blind people = problem maintaing normal 23 hour sleep wake cycle (no light dark cycle), for some, melatonin supplements = successful. 

• Circadian rhythm operate on a 24 hour cycle: e.g. human sleep-waking cycle, body temperature. 
• Endogenous pacemakers: SCN (superchaismatic nucleus) = a cluster of 10,000 neutrons in the hypathalamus. 
• Exogenous zeitgebers: light-dark cycle: 1) info about amount of light registered by retina, 2) sent via the retino-hypthalamic tract to the SCN 3) SCN cells fire and stimulate the pineal gland 4) produce melatonin. 
• Melatonin = sleep hormone - influences serotonin levels and the reticular activating system (RAS) which is responsible for inducing light sleep. 

• DETERMINSTIC: this explanation suggesting that sleep wake patterns are fixed/caused by internal/external cues = determinstic as it ignores cognitive ability however its possible to override the cues by training outselves to wake up early (Czeisler et al); APPLICATIONS. However Miles et al = case study of blind man = problems with daily life as he couldnt adapt his circadian rhythms to the depands of society. 
• CHRONOTHERAPEUTICS: APPLICATIONS: insight gained into daily hormonal fluctuations and sensitivity to pain have helped medical professions to highlight when it would be advantageous to take medication/recieve anaesthetic at certain times of the day. 
• INDIVIDUAL DIFFERENCES: everybody has different endogenous/exogenous circumstances; findings can't be applied fully. 

• Hublin Et Al (1997): sleepwalking more common in children - 20% affected compared to 2% of the adult population affected; SUPPORTING THE NEUROCHEMICAL explanation as it shows sleepwalking is linked to development/maturation as the explanation says that lack of GABA causes children to be common sufferers. 
• Lecendreux Et Al (2003): 50% concordance rates for sleepwalking in MZ twins and 12% in DZ twins; SUPPORTS THE GENETIC explanation as it shows that there is a genetic basis, however it is not the only factor as the concordance rates aren't 100%.
• Zadra Et Al (2008): experimental study - 40 participants prone to sleepwalking, number of sleepwalking behaviour counted on a normal night and then again after 25 hours sleep deprivation. On a normal night, 50% had shown sleepwalking behaviour however after sleep deprivation 90% showed sleepwalking behaviour; SUPPORTS THE ENVIRONMENTAL explanation as it shows that sleep deprivation increases sleepwalking behaviour but only in those genetically predisposed to the disorder. 

• Sleepwalking = parasomnia during sleep that doesn't result in daytime sleepiness, tends to run in families (some genetic involvement). No recollection of their actions when they wke up. 
• NEUROCHEMICAL EXPLANATION: Oliviero Et Al (2008): lack of neurotransmitter GABA (inhibits the motor system during sleep) may be involved as this GABA system develops slowly in childhood and is under developed in adult sufferers; links to why children spend more time in slow-wave sleep and why its more common in children. 
• GENETIC EXPLANATION: sleepwalking = incomplete arousal as EEG recordings have shown a mixture of delta waves (seen usually at NREM slow wave sleep) and beta waves (seen when awake); suggesting the person is awake but their brain isnt fully aroused; a genetic cause for this abnormal arousal has been found in twin studies. 
• ENVIRONMENTAL EXPLANATION: sleepwalking is caused by stress/alcohol/medication/sleep deprivation. 

• INDIVIDUAL DIFFERENCES: the neurochemical explanation ignores them as not all sleepwalkers have neurochemical abnormalities. 
• HIGH SCIENTIFIC: the genetic explanation as it uses accurate measurements like EEG to find that sleepwalking occurs in stages 3/4. Standard psychophysiological measurements like EEG are accurate and reliable. 
• DETERMINSITC: the genetic explanation says that sleepwalking occurs due to genes and ignores cognitive and environmental factors; IGNORES FREE WILL; can this be an excuse for inappropriate behaviour conducted during sleepwalking. 
• APPLICATIONS: the environmental explanation as there are risk factors that have been identified that may trigger sleepwalking episodes; people who are prone to sleepwalking can try to avoid these risk factors to lessen effects. 

• Van Goozen Et Al (1994): women undergo sex change to become male, recieve testosterone and become more aggressive; SUPPORTING the evolutionary approach as it shows that males are more aggressive and could have a genetic basis due to evolution. 
• William & Best (1982): gender roles in 30 cultures: men = dominant, women = nurturing; SUPPORTING as it shows that theres a universal agreement of gender roles. 
• Clark & Hatfield (1989): (48 m, 48 f) asked to have causal sex on an American campus, 75% males said yes, 0% females said yes; SUPPORTING the parental investment theory as it shows that women aren't motivated purely by sex as they have a longer parental investment (at least 9 months). 
• Buss (2010): meta-analysis with 30 cultures show that males are more sexually peomiscous; SUPPORTING the evolutionary theory; as it explains why males are more promiscous as they have less consequences of being promiscous. 
• Sternglanz & Nash (1988): found offspring were less likely to survive in the evolutionary past when males didnt stick around; CONTRADICTING the evolutionary theory which said males have less investment. 
• Thornhill & Palmer: natural history of **** (2000): **** is an evolved tactic enabling males who cant reproduce with consent to pass down their genes; ETHICAL ISSUES. 

• The evolutionary approach: gender differences occur because of selective pressures in the past that shaped different behaviours in men/women e.g. men had to hunt for food for the family; explaining why males are usually more aggressive. 
• Natural Selection: selection of behaviours/bodily features that allow an animal to compete successfully for food/shelter.survive. 
• Sexual Selection: selection of behaviours that allows an animal to compete successfully for mates/to reproduce, these processes ensured that behaviours that helped survival/reproduction for our ancestors were kept in the gene pool. 
• Parental Investment Theory: Trivers (1972): gender differences came from differences in parental investment: investment by the parent that increases the offspring's chances of survival at the cost of the parents ability to invest in other offspring. Qualities/behaviours that led to reproductive success were different for males (little parental investment) and females (at least 9 months). 

• SUPPORTING RESEARCH: males are 1.15 times larger than females; supporting as it shows that men being larger enabled them to compete succesffuly for food/ have access to females. 
• LOW SCIENTIFIC: as evolutionary accounts cant be tested as we cannot go back to see how  people behaved in the past; lowers the accuracy: Hagen (2002) said its an out of date approach. 
• DETERMINSTIC: doesn't allow for the variety of behaviours seen within each gender in everyday life; NURTURE IS IGNORED; however many studies have found that we are influenced by our environment on how we behave. 
• EVOLUTIONARY CONTINUITY: physical and behavioural continuity so it makes sense to compare humans with closely related animal species. There are universal principles concerning females as offspring bearers and males required for fertilation. 
• FREE WILL IGNORED: as behaviours are assumed to be determined by evolutionary adaptiveness so all humans have it. 
• REDUCTIONIST: stating that behaviour is only due to evolutionary purposes (long term) with no consideration of proximal (short term) causes of behaviour. 

• Deady Et Al (2006): link between high levels of testoserone in female salive and low desire to have a family; SUPPORTS as shows hormones affect behaviour. 
• Young (1966): gave male hormones to 1 group of pregnant rats and female hormones to another. Female offsprings exposed to male hormones = typical male behaviour (mount partner from behind), male with female hormones - typical female behaviour (lordosis position). SUPPORTS that horomes influence sexual behaviour. 
• Koopman Et Al (1991): genetic engineering to prenatally implant SRY in female mice; they were aggressive and mating behaviour; SUPPORTS as shows that the SRY gene is important in affecting gender behaviour. 
• Rommsayer & Troche (2007): measured 2D:4DR in 700 students, each participant masculinity/femininity score on BEM's SRI. Men with a feminine SRI had a female finger pattern; SUPPORTING that gender behaviour could be liked to biological causes like genes. 
• Swaab & Fliers (1985): SDN is 2.5 times larger in males from a sample of 31; SUPPORTING as it shows that structural brain differences between gender is caused by genes which control the release of testosterone which masculinises the brain; argued that the SDN is responsible for gender role behaviour. 
• Taylor (2000): oxytocin = nurturing. Kalat (2011): it triggers maternal instincts. 

• Biological approach: differences between genders occurs due to genes: males have XY chromosomes whereas females have **. On the Y, the SRY gene activates the SOX9 gene activating genes in the testes/brain masculinising the brain/body. 
• Ridely (2009) said this single gene determines the biological sex/ much of our gender role behaviour e.g. male = aggressive, females = nurturing. 
• Males produce in tesoterone in the testicles affecting the hypathalamus, enlarging INAH 1, 2, 3 = sexually dimorphic nucleus (SDN) making it larger.denser. 
• Females produce female horomes in ovaries that have little effect on the hypathalamus, the SDN remains small/not very dense. 
• Pinel (2010): male = testosterone = aggressive/dominant, females = oestrogen/oxytocin/progesterone = sensitive. 
• Chromosomal abnormalities: supermales **Y = taller, more aggressive, infertile. 

• ALPHA BIAS: sex differences are emphasies with researchers having a tendancy to look for differences rather than similarities; this means findings are bias. 
• REDUCTIONIST: skills and behaviour are broken down to differences in male compared to female brain regions. It is unlikely that gender differences are down just to one single chromosome: the SRY. 
• BIOLOGICALLY DETERMINSTIC: effects of nurture are ignores; this suggests that our behaviour and mental experiences related to gender are not changeable with the hold of genetics over our development being too powerful. 
• IGNORES FREE WILL & COGNTIVE ABILITY as it shows that our genes and horomes dictate our gender behaviour however it is unlikely that gender differences are down to just biological factors as its been found that environmental factors also effect development. 
• HIGH SCIENTIFIC as well established technqiues have been used to measure bits of the brain such as the SDN in males and females. 

• Toh Et Al (2001), Xu Et Al (2005): genetic research, identified 2 mutations linked to the control of circadian rhythms: people with these mutations = more likely to suffer from insomnia than the control group; SUPPORTS THE GENETIC person has a genetic mutation = develop this disorder. 
• Ridley (2008): clear genetic link for insomnia found in research, findings indicate the disorder runs in families; SUPPORTS THE GENETIC as it shows maladaptive genes are inherited. 
• Dauveilliers Et Al (2005): compared insmoniacs with a control group, 72.7% of sufferers reported a family history, 24.1% of the sufferers reported a family history; SUPPORTING THE GENETIC as genes play a role in the disorder.
• Watson Et Al (2006): twin studies have shown a genetic link for insomnia and also suggested that genetic factors lead to hyperarousal and insomniacs are more likely to experience hyperarousal day and night; SUPPORTING THE GENETIC: shows genetics play a role. 
• Furukawa (2009): success in using behavioural treatments to address personality linked insomnia; SUPPORTS ENVIRONMENTAL: as it shows maldaptive learning experiences may be an important factor. 

• Insomnia: problems with quality/duration of sleep leading to daytime sleepiness. Symptoms: sleep onset latency (time taken to fall asleep) more than 30 minutes, sleep efficiency less than 85%, increased night time awakenings. 

GENETIC EXPLANATION:

• Insomnia is a genetic disorder, genes are inherited which lead to a person suffering with insomnia (absolute genetic explanation) or which can predipose the person to insomnia but only develops if other factors interact (genetic predisposition explanation). 

ENVIRONMENTAL EXPLANATION:

• The behavioural approach explains insomnia through classical conditioning, sufferers may have learned to associate alertness/active thinking/stress with bedroom environment because they used the bedroom as a place to eat/work/watch TV/discuss problems; associated with activity. Insomnia maintains as they further associate lack of sleep and anxiety in the bedroom. 

• LOW ACCURACY: Dement (1999): studies suffer from sleep state misperception: particpants under/over report the amount of sleep and family histories may not be accurate. 
• HIGH SCIENTIFIC VALIDITY: well establushed scientific methods to find e.g. concordance rates are used. 
• SUPPORT FOR THE GENETIC PREDISPOSITION theory as its suggested that genetic factors predipose an individual to suffer from insomnia. Environmental triggers the disorder e.g. the expections of not being to sleep because of stress and can lead to a self-fulfilling prophecy. 
• APPLICATIONS: using BEHAVIOURAL principles, the association can be unlearnt like only using the bedroom to sleep; new association. Also increaseing sleep hygiene such as less naps/drinking and eating late cause the circadian sleep wake cycle rhythm not to be dysnchronised. 
• INDIVIDUAL DIFFERENCES aren't considered as why a person may suffer from primary insomnia is hard to conclude, as much of the evidence is anecdotal, it LACKS EMPRICAL EVIDENCE. 
• NOT FULLY EXPLAINED as its unsure whether insomnia is a symptom of another cause (secondary) or a disorder (primary); anxious person has increased chance of insomnia; could be symptom. CBT is successful in reducing this. 
• HOLISTIC EXPLANATION as it's impossible to explain without considering nature & nurture. 

• Meddis (1975): sleep is to keep animals safe when active behaviour is impossible CONTRADICTS: makes sense for animal to be awake/alert rather than asleep

• Allison & Cicchetti (1976): sleep patterns in 39 species: prey = sleep less than predators; CONTRADICTS Meddis. 

• Lesku et al (2006) pointed out that prey are usually herbivores;need more time to stay awake to find/eat food

• Webb (1982): sleep = conserve energy especially small animals that burn energy quickly due to high metabolic rates: SUPPORT: positive correlation: metabolic rate and sleep time.
• Alcock (1993): reviewed literature of sleep patterns in animals: those that eat often/vulnerable to predators have little sleep (cattle), those that eat once a day/few predators sleep lots (cats). Small animals that need less food/protected when sleeping (sleep in caves like bats) spend time asleep. SUPPORTS shows that sleep serves purpose of keeping animals safe/increase survival chances.
• Pinel (1983): evolutionary better than restoration theory of widespread between species difference in amount of sleep: Restoration: animals that use more energy should sleep longer but no relationship between body size/sleep e.g. gian sloth sleeps for 20 hours; CONTRADICTS RESTORATION. Evolutionary: sleep related to vulnerability/survival needs: e.g. zebra sleeps 3 hours and grazes continously but lions sleep for 2/3 days after a large kill; SUPPORTS EVOLUTIONARY as it shows animals who sleep a lot usually do because they can survive and have resources to do so but also CONTRADICTS: sleep=essential. 

• Evolutionary = sleep occurs to avoid predation/conserve energy: the evolutionary survival function in an animals ecological niche, specific sleep patterns evolve. 
• Ecological niche/nutritional needs influence how much/when animals sleep.
• Neural Mechanisms have evolved to encourage animals to sleep when they don't need to engage in behaviour necessary for their survival/vulnerable to predation. 
• Sleep has evolved for conserving energy/keep safe from predators. REM evolved to maintain brain tempature as it could drop low (brain active = REM). Evolved sleep patterns to match their ecological nich e.g. bottlenose/indus dolphin sleeps with half their brain active at 1 time for survival.
• Ancestral past: babies sleeping = mothers can engage in behaviour needed for survival. 

• ANIMAL STUDIES: many studies conducted on animals; cannot generalise all e.g. we can generalise that sleep is for energy conservation but we cannot generalise the importance of safe sleep site. 
• NATURE & NURTURE: both are considered as ecological and physiological factors are mentioned. 
• REDUCTIONIST: as it ignores situational factors as the theory says it has a genetic basis however no genes have yet been identified linked with difference in animals in sleep. 
• LOW SCIENTIFIC VALIDITY as there isn't much proof, however just because there is no proof yet, it doesn't mean that there aren't genes that cause difference in sleep in animals. 

• Mead (1935): ethnographic research of gender roles in 3 cultural groups in New Guinea, differences she found she argued were due to social factors (cultural norms/socialisation) and says biological factors have no influence. Munduagumor = men/women socialised to be aggressive/emotionall unresponsive. Arapesh = men/women were caring/non aggression. Tchambuli = gener role reversal compared to western cultures: males = sensitive, females = dominant. SUPPORTS NURTURE as it shows gender roles aren't universal and social factors effect gender development. 
• Ember (1981): boys = more competitveness/aggression than girls. 
• Omar Et Al (1975): similar pattern as Ember in playground observations in Switzerland/Ethiopia/USA: CONTRADICTS MEAD: gender differences due to nature too. 
• William & Best (1990): 30 cultures, questionnaires to 2800 students: universal agreement accros cultures about whats masculine (aggressive) and feminine (nurturing): CONTRADICTS cultural-social  approach as it suggests that gender behaviour is universal. 
• Whiting & Whiting Et Al (1988): cross-cultural study: natural environments in US, Japan, Kenya, India, Philippines, Mexico: key differences between genders same accross all cultures: girls (nurtuing) boys (dominant). However boys = more time with fathers, encouraged to achieve more/be independent - more differences in India, Mexico, Japan (girls do housework) than USA, Kenay and Philippines. SUPPORT FOR NATURE & NURTURE. 
• Bee (1995): gender role differences due to brought up e.g. girls = responsible early. 

• Behavioural approach: we learn gender through socialisation/upbringing through:
• Operant conditioning which is providing positive reinforcement for some behaviour (e.g. boys play with cars) and negative reinforcement for others (e.g. boy plays with doll).
• Social Learning Theory: observation of same sex role models and imitations of their behaviour when it's seen to bring rewards (vicarious reinforcement). 
• In young children: main role models = parents/older sibilings, later they observe peers too. SLT occurs through media also. 
• Self efficacy is also a factor influencing imitation: high self efficacy = more likely to imitate a role model than if they have low. 
• Peoples culture also has an impact on gender role: behaioural approach says gender behaviour varies accross the world due to different cultural influences. 

• DETERMINSTIC: as it ignores nature aspects if gender development but its been proven that genetics and hormones such as testosterone affect gender. Biologically selcted preferences are difficult to change.
• REDUCTIONIST: by not considering nature it only looks at gender development through socialisation and culture however there are findings that differences such as chromosome differences in gender have proven that there are biological factors affecting gender. 

• Drummond: 30 girls at GD clinic age 2-3. Followed up at age 7 & 18. Age 18: 88% had lsot the symptoms but 12% wanted to undergo surgery; SUPPORTING the biosocial approach that states social factors like labelling = more influential than biological factors. 
• Drummond Et Al (2008): many transgenders showed cross-gender preference in toys/games/clothing in early childhood; he argued learning experiences interact with genetic predisposition; SUPPORTING biosocial as it predicts both nature & nurture affect gender. 
• Coolidge Et Al (2002): meta-analysis: 62% of symptoms due to biological and 32% due to social; CONTRADICTING: biosocial as it focused more on social factors not biological. 
• Glicksman (2013): much of the evidence/theories on causes for GD is based on transgenders who dont meet the DSM-5 diagnostic criteria for GD as they dont have the same distress/impariment. 
• Hines (2004) people with GD have strong desire to change sex despite social/biological obstacles; GD is universal: suggests a biological influence; CONTRADICTS the biosocial. 

• Biosocial approach: Money & Erdhardt (1972): gender develops from interactio between biological & social factors.
• Biological factors like gene/hormones cause genetic sex (based on chromosomes) and controls production of hormomes causing charcteristics.
• Social factors start from birth with labelling baby as boy/girl: through socilsation/environment (parents/peers) and cultural views. 
• Gender dysphoria = belief you're trapped in the wrong body, biosocial approach says that biological factors (genes) predipose certain people to GD but only manifests itself when certain social factors occur like an absent parent during the phallic stage/maladaptive learning/schema.
• Psychodynamic approach suggests that a failure to resolve the oedipus/electra conflict during the phallic stage can cause GD. Stroller (1969) points to extremely close mother-son relationships to be caused by asbent fathers to cause strong identification with the mother in young males; leading to a reversal of expected gender roles. 

• The psychodynamic approach can be considered as biosocial to GD as both NATURE & NURTURE are considered: stages of psychosexual development are univesal (genetics) and a child's experiences during the phallic stage determine the outcome of the oedipus/electra conflict; SUPPORTS the biosocial. 
• LIMITED SAMPLE: many studies used transgenders rather than gender dysphoria sufferers. 
• ETHICS: debatable whether children should be encouraged to confrom to gender stereotypes. 
• Just because someone shows stereotypical opposite gender behaviour does this mean they have GD or INDIVIDUAL DIFFERENCES IGNORED. 
• ETHICS: should a child be treated for GD as Drummon showed that symptoms could change. 
• NATURE & NURTURE considered; HOLISTIC explanation. 
• Baby X study provides SUPPORT as it shows when babies dressed in non specific gender clothes and labelled as boy/girl; adults played according to gender label not temperament; social factors influence gender. 

• Wilson Et Al (1995): women who described their husban on a questionnaire as jealous and not wanting them to talk to other men = twice as likely to have experienced violence, 56% scared for life, 72% requiring hospital treatment; SUPPORTING that jealousy is caused by the threat of infidelity as a product of an adaptive response. 
• Shackleford Et Al (1995): 1461 m, 560 f, males answered questions how they stopped their wives from being unfaithful/how often they were violent/direct guarding. Women were asked about their partners behaviour. A positive correlation between direct guarding and the frequency of violent acts; SUPPORTS that due to threat of infidelity; partner becomes aggressive, those who are more vigilant towards infidelity=more jealous=more aggressive to prevent it = male retention strategy.
• Kaighobadi Et Al (2008); 165 males: questionnaire: how often they accused their partner of infidelity and sued retention strategies (turning up unexcpected) and violence. As accusations increased so did retention strategies and violence; SUPPORTS as indicates as aggression occurs as a reaction of jealousy caused by threat of infidelity. 
• Daly & Wilson (1998): male-male aggressive rivalry occured in almost all cultures; cross cultural evidence SUPPORT. 

• Evolutionary: aggression is an adaptive response, it serves an important function for survival/increases reproductive success. 
• Infidelity can pose a threat to individuals reproductive success and surivval, in order to reduce jealousy caused by threat of infidelity, individuals become aggressive: intra-sexual (against same sex) or inter-sexual (against opposite sex). 
• Female: certain an offspring is hers; males are worried about infidelity as they're not sure they're investing into their own offspring (genes). 
• Women: more concerned with emotional infidelity: if partner forms emotional relationship with another: they may stop investing time/resources into them and their offspring; reducing survival chances. 
• Threat of infidelity and jealousy, to attempt to reduce infidelity causes aggression. 
• Females: verbally aggressive towards other females (criticise appearance) aiming to reudce competition for males, deters their partner from being unfaithful; increasing reproductive success. 
• Males: aggressive towards other males to reduce competition for mates; increasing reproductive success and also attracts mates by showing they're capable of protecting them. 

• REDUCTIONIST: oversimplified as jealousy doesn't always lead to aggression; its argued that human relationships are more complex and other factors should be considered like stress/diet/smoking. Also IGNORES NURTURE & EMOTIONS. 
• DETERMINSTIC: this theory says aggression is inevitable due to survival instincts but its argued that individuals do have control over their behaviour and we should take responsibility for our actions; shouldn't be used as an excuse; FREE WILL SHOULDN'T BE IGNORED. 
• CAN'T DRAW FIRM CONCLUSIONS: as many of our instinctive behaviour (aggressive/sexual urges) have to be controlled due to society rules; hard to measure accurately. 
• LOW SCIENTIFIC: as lacks empirical evidence as we cannot test the theory by going back in time. 
• APPLICATIONS: male retention strategies are indicators of potential violence; counselling can prevent this. 

• Evans & Rowe (2002): xenophobia is an irrational dislike of people from other countries that arises from over exaggeration of the threat of the out-group. Analysed police interview/post match reports/official reports from 40 football matches in Europe with English clubs/national teams. Higher level of aggression found when English national team played another team because the English team is less ethnically diverse and supporters are more xenophobic; SUPPORTING as shows that being cautious/aggressive towards another team = beneficial for survival as its argued that xenophobia is favoured by natural selection as its allowed our ancestors to avoid harm by potential threat = reproducitve success. 
• Foldesi (1996): Hungarian football crowd: racist chants/banners led an increase in spectator violence; the xenophobic abuse often aimed at Russains/former Yugoslavians/Romanians: SUPPORTS as it argues that this behaviour is adaptive as the aggression is aimed at the other group who pose a threat to resources like (territory). 
• Clark Et Al: research in Brazil, Sao Paulo, percentage of Afro-Brazillians was negatively correlational with lynch mob incidents; Afro Brazillians posed no threat economically/politically yet were targets of lynch mobs; CONTRADICTS the power threat hypothesis as it states aggression when they threat group survival, but they didnt. 
• Dunning Et Al (1998): argued that sports violence isnt harmless as verbal aggression turns to physical and could result in injury; CONTRADICTS: as it suggests that aggression as a sporting event actually threatens survival chances; not increases. 

• Alliances provide advantages in terms of protection/ensuring vital resources (food/protecting territory/offspring). It's argued that those who show more aggression have more reproductive success. Alliances create an in-group (remain dominant) who are aggressive towards the out-group. It is suggested that it's more adaptive to exaggerate the nergative stereotypes of the out-group as being over cautious about the threat they posse will be less costly to an individuals survival. 
• Group displays of aggression = ritualistic: as they strengthen the in-groups membership and intimidate the enemy. Aggressive behaviour at sporting events = ritualistic (verbal/no physical) shows unity but doesnt risk injury; makes enermy aware they have power to defend themselves.
• Power-threat hypothesis: groups who pose a threat to a majority survival = likely to be discriminated e.g. lynch mobs were due to "threat" of homicides by blacks against the white majority; this "justified lynching"?
• Cold war: mutually assured destruction; both US and USSR knew they had enough nuclear weapons to destroy the world; tried to avoid using them by making the enemy aware they had the power to destroy the other side through propaganda (verbal abuse). 

• LOW SCIENTIFIC: as the theory is based on the idea that aggression has developed for survival and passed through generations; cannot be objectively tested. 
• APPLICATIONS: could benefit to society to reduce aggression at sporting events; if physical aggressive rituals at sport events like chanting were cutrailled then Marsh says levels of physcial violence would increase; ritualistic behaviour should remain. 
• IGNORES FREE WILL: shouldnt justify unacceptable behaviour like lynching due to the 'threat' to a majority survival. ETHICS. 
• DETERMINSTIC: if aggressive ritual behaviour is evolutionary/biologically determined, it's out of the individuals control. 
• REDUCTIONIST: behaviour is reduced down to its evolutionary functions; IGNORES COGNITIVE ABILITY. 
• CULTURAL BIAS: when interpretting data from other countries e.g. Hungary, researchers interpretations likely to be influenced by the views of their own culture. 
• ALPHA BIAS: adaptive explanations exaggerate aggression differences between males and females, doesn't look closely at similarities. 

• Dement & Kleitman (1957): 9 participants in sleep lab for up to 61 nights, EEG used to wake them up at different stages of sleep: found 2 types of sleep. Woken during REM = 90% dreaming and 7% in NREM. REM periods, every night for 3-50 minutes. Provides INSIGHT that dreaming occurs mainly in REM. 
• Green (1999): 30% reported dreaming in NREM; CONTRADICTS Dement & Kleitman who said very little (7%) dreaming occurs in NREM. 
• Cultural Study: 11-12 year olds: Israeli children sleep for 9 hours and Swiss for 10 hours; suggesting cultural/individual differences affected by environmental factors. 
• Van Cauter Et Al (2000): 149 healthy males age 16-83, 14 year study: majority over the age of 45 has less slow wave sleep (4 NREM): leading to loss of muscle mass/decline in ability to excercise making partake pants more prone to obesity; SUPPORTS that older adults sleep length gradually decreases with age and stage 4 NREM disappears due to growth hormones released at this stage of sleep; growth/repair also slows down. Elders sleep for 6 hours; sleep pattern = fragmented/engage in more daytime napping; poor alertness. 
• Siegel (2003): relationship between neural development and REM. Platypus: brain immature at birth = 8 hours of REM but dolphin swims from birth has no REM; SUPPORTS that REM is essential for brain growth. 

NATURE OF SLEEP:

• Sleep = part of the 24 hour circadian sleep-wake cycle: lowest measurement in conscious awareness and physical activity. 2 types of sleep = REM or NREM. Sleep is an ultradian rhythm as theres cyclical variations as we go through NREM and enter REM. Sleep = active neurological process: 
• SCN/pineal gland responsible for sleep onset Raphe nuclei/ serotonin in influencing NREM RAS lowers cortical activity during NREM   Locus coereleus/acetylcholine in initiating REM. 
• Darkness: pineal gland makes melatonin affecting brain cells that makes serotonin influencing mood/sleep behaviour. Serotonin accumulates in the raphe nuclei near the pons; stimulating the shutting down of the reticular activating system (RAS). 

LIFESPAN CHANGES:

• EEG/EOG found that REM decreases with age: premature babies: 90% in REM, newborn 16 hours sleep 50%, 1 year olds 12 hours sleep : 35%, adults 8 hours sleep: 20%. EEG shows that time spent in stages 3/4 reduces by 50% compared to the age of 20. At 90, they dont occur. 
• EEG shows infants have shorter sleep cycles/awakening during infancy/age 60+ are more frequent as their ultradian cycles are shorter than 90 minute cycles in adults. 

• STAGE 1 NREM: lightest sleep, EEG charcterised by theta waves. 
• STAGE 2 NREM: light sleep, still responsive to external stimuli, bursts of sleep spindles/k complexes. 
• STAGE 3 NREM: deep sleep, unresponsive to external stimuli, only a few minutes, delta waves appear and spindles disappear. 
• STAGE 4 NREM: very deep sleep, 30-40 minutes, delta waves occupy over 50% of the time. This is when sleepwalking occurs. 
• STAGE 5 REM: brain waves active but body paralysed for 10-15 minutes, completes the first cycle of the night. 80% of dreams occur in REM. 
• Cycle repeats every 90 minutes but time in stages 3/4 decreases till only stages 1/2/5 are entered. 

• HIGH SCIENTIFIC: using measurements like EEG which are well established provides reliable and accurate results. 
• LOW ECOLOGICAL: sleep labs aren't the same as when sleeping in natural settings at home; can't generalise as participants may have difficulty sleeping in the sleep labs. 
• INDIVIDUAL DIFFERENCES: there are individual differences in sleep such as even age being an endogenous pacemaker; findings cannot be generalised to all ages. 

• Siffre (1975): 179 days in cave - Texas, no external zeitgebers, sleep wake cycle = 25-32 hours, body temperature = 25 hours. SUPPORTS that absence of natural light-dark cycle; body clock can regulate circadian rhythm but not accurately. 
• Aschoff & Wever: students in underground bunker, no light cues, sleep wake cycle = 24-27 hours; SUPPORTS that endogenous pacemakers can control the sleep wake cycle. 
• Ralphe & Menake (1990): mutant hamster with 20 hour sleep wake cycle, SCN transplant with a 24 hour hamster, hamster adopted the donors sleep wake cycle. SCN was destroyed, circadian cycles = random; SUPPORTING that the SCN is the main endogenous pacemaker. 
• Lews & Lobban (1950's): participants in Arctic circle, unknowingly had their watches set to 21/27 hours. Constant light; no exogenous zeitgebers (light-dark cycle); participants sleep wake cycle operated to their watches; SHOWING that zeitgebers can override the natural 24 hour circadian biological clock. 
• Folkard Et Al: gradually reduced circadian rhythm with a quickening clock, but at 22 hours, participants own rhythms took over again; CONTRADICTS Lewis & Lobban as it shows that endogenous pacemakers cant be completely overriden by external zeitgebers. 
• Russel (1980): pheromones applied to group of 5 sexually inactive women: the donor's odur applied to lip of each participant daily for 5 months: 4/5 synchronised to within 1 day; SUPPORTS that pheromones as an exogenous factors can affect the menstrual cycle.  McClintock & Stern (1998): 29 women with irregular periods, replicated Russel's study for 10 years, 68% responded to pheromones and cycles changed by 14 days. 

• Circadian rhythm operate on a 24 hour cycle: e.g. human sleep-waking cycle, body temperature. 
• Endogenous pacemakers: SCN (superchaismatic nucleus) = a cluster of 10,000 neutrons in the hypathalamus. 
• Exogenous zeitgebers: light-dark cycle: 1) info about amount of light registered by retina, 2) sent via the retino-hypthalamic tract to the SCN 3) SCN cells fire and stimulate the pineal gland 4) produce melatonin. 
• Melatonin = sleep hormone - influences serotonin levels and the reticular activating system (RAS) which is responsible for inducing light sleep. 
• Ultradian rhythm = biological rhythm that occurs more frequently that once every 24 hours e.g. alternation between NREM and REM. 
• Age is an endogenous pacemaker as REM decreases with age; affects sleep. 
• Infradian rhythm = occurs more than 24 hours e.g. menstrual cycle. 
• Endogenous pacemakers: pituitary gland releases hormones and regulates the endorcrine system which secretes hormones into the bloodstream; increasing oestrogen/progesterone levels to prepare the uterus for pregnancy. 
• Exogenous zeitgeber: light influences menstruation and the production of melatonin, stress also influences menstruation. 

• DETERMINSTIC: this explanation suggesting that sleep wake patterns are fixed/caused by internal/external cues = determinstic as it ignores cognitive ability however its possible to override the cues by training outselves to wake up early (Czeisler et al); APPLICATIONS. However Miles et al = case study of blind man = problems with daily life as he couldnt adapt his circadian rhythms to the depands of society. 
• CHRONOTHERAPEUTICS: APPLICATIONS: insight gained into daily hormonal fluctuations and sensitivity to pain have helped medical professions to highlight when it would be advantageous to take medication/recieve anaesthetic at certain times of the day. 
• INDIVIDUAL DIFFERENCES: everybody has different endogenous/exogenous circumstances; findings can't be applied fully. 
• NATURE & NURTURE both considered as both factors external and internal are mentioned in the explanation. 
• HIGH SCIENTIFIC: use of EEG/EOG/EMG have increased the reliability of findings e.g. K complexes have led to the conclusion that noise is an exogenous zeitgeber influencing ultradian rhythms. 

• Tryon (1940): selective breeding in rats: observed behaviour and divided them in an aggressive group or docile group. Over 26 generations: aggressive rats produced aggressive offspring and docile rats produced docile offspring; SUPPORTING the absolute genetic explanation as it shows gene for aggression is inherited. 
• Brunner Et Al (1993): dutch family where males had a mutant form of the MA0A gene: resulting in absence of MA0A enzyme; reacted angrily and many had been involved in extreme aggression (****/arson); SUPPORTS that abnormal MA0A activity caused by a single gene affects aggression; supporting the absolute genetic explanation. 
• Berkowitz (1993): MZ twins have 75% concordance rate for aggression, DZ twins have 24%; suggesting that the more genetic mateiral 2 individuals share, the more similar the levels of aggression; SUPPORTS the genetic predisposition as it shows theres a genetic basis. 
• Mednic Et Al (1984): 14000 adoptees all criminals: 14% had neither adoptive/biological criminal parents, 20% had biological criminal parents, 25% had both adoptive and biological criminal parents; SUPPORTS the genetic predisposition as children who didnt grow up with biological criminal parents were still more likely to be criminals; suggesting that aggression has a genetic basis. 

• Absolute genetic explanation: some individuals inherit a maladaptive gene/or combination of genes (polygenic) which causes aggression like the MA0A explanation: 
• The MA0A gene on the X chromosome is implicated in aggression - it produces an enzyme which breaks down excess levels of neurotransmitters (serotonin/noradrenaline/dopamine). Research shows that people/animals with an underactive MA0A gene are associated with high levels of aggression:
• Under active MA0A gene = low levels of MA0A enzyme = high levels of serotonin/noradrenaline = aggressive behaviour. 
• The genetic predisposition explanation says that people with maladaptive genes have higher chance of aggression but only develops when interactive with other factors. 

• REDUCTIONIST: the absolute explanation has been criticised for oversimplifying the cause of aggression as it reduces the complex behaviour down to just 1 gene: the MA0A gene. Many argue that there is strong evidence for aggression being caused by an interaction of both external and internal factors. 
• FREE WILL: if aggressive behaviour is genetically determined like the absolute explanation says then it is hard to blame the individual for their behaviour as it could be outside their control; free will shouldn't be ignored and shouldn't provide an excuse for unacceptable behaviour like murder due to an aggressive gene. 
• NURTURE IS IGNORED: the absolute explanation states that aggression depends just on biological factors however it's been proven that environmental factors also effect aggression. 
• BETA BIAS: the studies claim that males and females are affected by genes in the same way however it is unlikely that males and females are affected in the same way.
• CULTURAL BIAS: effects of culture upon behaviour is not considered, most studies find data only from western cultures, the findings cannot be generalised to other cultures where they have different mentalities and views. 

• Bandura Et Al (1961): showed children adult playing aggressively with bobo doll, after 20 minutes, the children showed more aggression towards the bobo doll than the control group. 
• Bandura (1965): 66 children from nursery Standford University: chilrdern who observed model being rewarded for being aggressive with bobo doll became most aggressive, next was those who saw no reinforcement, the least aggressive were those who saw the model being punished: SUPPORTS as aggression can be learnd through vicarious reinforcements. 
• Anderson & Dill (2000): independent measures: 200 American college students: those who played violent video games used longer blasts of noise to punish the opponent than those who played non-violent games: SUPPORTS that aggression can be learned through operant conditioning as video games rewards aggressive behaviour with points. 
• Williams (1986): physical aggression increased more in 6-11 year olds who'd never seen Tv before in Cananda rather than those who'd already had 1/several channels. Peers and teachers rated their aggression. SUPPORTS that we learn aggression through obersvation and imitating it. 
• Jamie bulger case study: murdered by 2 males aged 10 and 11 who had seen child play 3 before the incident: SUPPORTS that media affects aggression. 

• SLT argues that aggression is learned through: 
• Direct observation: paying attention to behaviour of role models. The individuals ability to observe and store the information depends on how likely they are to imitate the behaviour. 
• Reinforcement: when we're positively reinforced, it is likely we'll repeat this behaviour more than when we are negatively reinforced - this motivates us to behaviour or not to behave like the role model.
• Operant conditioning: indirect learning: when observing the role model, if the role model is being rewarded for their aggressive behaviour, this may cause the child to imitate the behaviour - vicarious reinforcement. 
• The status of the role model effects chances of imitating the behaviour, so if the child sees their parent acting aggressively then they're more likely to act aggressive than seeing a stranger repeat the behaviour. 
• Self efficacy will affect the likeliness of imitating aggression, aggressive behaviour can have disastrous consequences; those who are less confident will not act as aggressively in the future. 

• APPLICATIONS: SLT can be applied to other areas of antisocial behaviour and has taught parents the importance of making sure children watch/play age appropriate films and games. 
• DETERMINSTIC: passively imitate the witnessed behaviour with no prior logical though; ignores cognitive ability. 
• REDUCTIONIST: biological factors are ignores ike hormones but its been found that testoserone is likely to cause an individual to be more prone to aggression. 
• SLT seens aggression as an option whereas the psychodynamic approach says it is unavoidable; FREE WILL is considered and a person is responsible for their actions. 

• Lytton & Romney (1991): meta-analysis of 175 studies, 28000 partcipant: found no difference in amount of communication/interaction that parents had with boys/girls. In North America, boys were encouraged to do outdoor tasks, girls to do indoor tasks. In Western countries other than US, boys were more likely to be physcially punished than girls. Fathers more likely to treat boys/girls differently; SUPPORTING that parents influence gender development. Siegel (1987): fathers are more likely to correct boys when playing with girls toys. 
• Durkin (1995) & Harris (1998): argue that peers play more of a role than parents in gender shaping; CONTRADICTING Siegel and Lytton & Romney. 
• Lipps (1997): reviewed literature: concluded that parents are the most important influence on gender roles until the age of 10. 
• Fagot (1985): 2 year old boys/girls criticise their peers for gender inappropriate behaviour and reinforce appropriate behaviour; SUPPORTS that operant conditioning occurs. Fagot found that parents do the same thing before the age of 2. 
• Fagot (1992): 27 egalitarian families and 42 traditional. At age 4, the traditional familiy children produced more stereotypical answers; SUPPORTING that gender behaviour is absorbed through role models. 
• Thompsom & Zerbinos (1997): 4-9 year olds described cartoon characters as males as aggression and females as domestic: SUPPORTING that the media has an impact. 
• Baby X Experiment: Smith & Lloyd shows how parents influence behaviour as babies were treated by adults depending on label rather than temperment. 

• McConaghy (1979): doll in transparent clothes, 3-4 year olds decided dolls gender based on clothes; SUPPORTS Kohlberg as it accurately identifies the ages at which children gain different kinds of understanding; gender stability, using superficial sign e.g. dress=girl. 
• Munroe Et Al (1984): 3 stages were similar in 6 cultures including: USA, Kenya, Nepal, Belize, Samao; SUPPORTS as shows the 3 stages are universal (based biological maturation).
• Slaby & Frey (1975): 2-5 year olds in high and low gender constancy groups shown a silent film with 2 adult models. Split screen model, child was able to watch both films at same time (male changing tyre/woman baking). Eye movements/direction/length of gaze measured. Children with high GC paid attention to same sex role model; SUPPORTS as shows once child has reached GC it would observe same sex role models and imitate them.
• Ruble (1981): relationship between GC and children's responsiveness to TV adverts for 'girls' and 'boys' toys. Those who'd reached GC were sensitive to implicit messages that certain toys were right/wrong. They found willingeness to play with toy advertised depended on how 'gender suitable' they felt it was; SUPPORTS as it shows those who reach GC begin to understand and develop schemas based on environmental factors like the media. 

• Cognitive approch: children dont come into the world with masculine/feminine behaviours, gender roles develop as their understanding of the world does too. Cognitive theories focus on child's thinking of what it is to be male or female. 
• Kohlberg shows how children's understanding of gender increases with age in 3 stages linked to age and we go through the stages based on environmental factors. Children show differences in behaviour when GC is reached as we develop schemas through scoial factors and imitate same sex role models - this is self socialisation. 
• Stage 1: Gender Identity: age 2-3 understand own gender but not that it's permanent. 
• Stage 2: Gender stability: age 3-5: know sex wont change but used superficial signs such as short hair = boy. 
• Stage 3: Gender constancy: age 5-7: no longer use superficial signs - this is conservation. 

• NATURE & NURTURE both considered as the stages are universal; biologicall determined and experiences determine how they progress through the stages. 
• Gender schema theory by Martin & Halverson says that children pay attention to same sex models earlier than Kohlberg predicted, they construct simple schemas by the age of 2 which makes them pay attention to same sex role models. This CONTRADICTS Kohlberg who says that self socialisation and imitating same sex role models happens once GC is reached at age 7. 
• FREE WILL is considered as children are said to play an active role in their gender development, allowing them to have a lot of influence in controlling their masculinity/femininity; providing change through selc socialisation. 
• REDUCTIONIST: the complex interactions of mental processes is oversimplified into time allocated phases; IGNORES INDIVIDUAL DIFFERENCES; so children can go through the stages at different ages. 

• Smith & Lloyd (1978): baby X experiment: dressed babies in non- specific gender clothes and labelled them as boy/girl names. They found that adults played with them according to their gender labels rather than temperament; SUPPORTING that labelling affects gender. 
• Condry (1976): 200 adults shown (same) video of a child labelled David or Dana playing with a jack in the box which caused the child to cry. Adults decribed David's behaviour as anger but Dana's behaviour as fear; SUPPORTS as it shows the importance of gender labels.
• Bradley Et Al (1998): case study of biological boy with surgery and raised as a girl; although she showed some male behaviours as a girl, she preferred female company and was happy with her female gender identity; SUPPORTING as it suggests socialisation can override biological sex. 
• Reiner & Fearhart (2003): 16 biological males - surgery and raised as girls, some showed male gender role behaviours and 10 deccided to change back to male; CONTRADICTING the biosocial as it shows biological factors are more important. 

• Vogel (1960): recorded the neural activity in the brainstem of narcoleptic dogs, they found that cataplexy is linked the activation of cells that in normal animals are only active during REM; SUPPORTS the biological explanation as it shows that narcolepsy symptoms cataplexy is linked to REM. 
• Thannickal Et Al (2000): found that orexin producing cells in the brain are reduced in people with narcolepsy; SUPPORTING the biological explanation as it shows that mutations on chromosome 6 and deficiency in brain proteins orexin/hypocretin play a role in sleep patterns. 
• Lin Et Al (1999): studied dogs for 10 years and identified a link between the neurotransmitter hypocretin and narcolepsy. Hypocretin's are thought to play a specific role in wakefulness. They studied narcoleptic dogs that had a genetic mutation on chromosome 12 which is thought to have disrupted the processing of hypocretin. The findings can explain why some but not all sufferers have low hypocretin levels as the 10% of sufferers with normal levels of the neurotransmitters may have faulty hypocretin receptor sites in the synaps: showing that the role of neurotransmitters in the sleep disorder narcolepsy is important and offer a variety of explanations for why there may be a faulty hypocretin systems or low levels of hypocretin in sufferers of narcolepsy; SUPPORTS the neurotransmitter explanation that theres a link between the genetic explanation and the neurochemical explanation of narcolepsy. 
• Its been found that a detective gene  (hypocretin receptor 2) has been identified in dogs also occurs in humans.

• Narcolepsy symptoms: extreme daytime sleepiness/cataplexy: the sudden loss of muscle tone awake/hypnagogic hallucinations: dreamlike experiences occuring during wakefulness/sleep paralysis. 

BIOLOGICAL EXPLANATION:

• Malfunction in brain areas responsible for sleeping/waking and in particular a dysfunction in the onset of REM. Sufferers go directly into REM and miss out the period of REM where they would've experience a deep sleep. This could explain why the sufferer doesn't feel rested when they've been to sleep. 
• Symptoms like cataplexy may occur when REM (paralysis/dreaming) intrudes into wakefulness. 

NEUROTRANSMITTER EXPLANATION:

• The role of neurotransmitters in the sleep disorder narcolepsy is important and offer a variety of explanations for why there may be a faulty hypocretin systems or low levels of hypocretin in sufferers of narcolepsy. 

• The explanation that narcolepsy and cataplexy are caused by REM dysfunction has recieved LITTLE SUPPORT; is no longer accepted as a valid explanation as it's outdated and the EXACT CAUSE of narcolepsy is unkown. 
• The biological explanation hasn't been explained by genetic factors in humans; concordance rates in twin studies and the ability to identify genes linked to the disorder have been unsuccessful. Its suggested that low levels of hypocretin could be caused by exogenous factors like diet or stress; NURTURE NEEDS TO BE CONSIDERED; otherwise this approach could be considered as REDUCTIONIST and DETERMINSTIC.
• GOOD FACE VALIDITY: as the neurotransmitter explanation is accepted and supported by lots of research. Recently the biological explanation of narcolepsy have overtaken the very poorly supported explanation that narcolepsy was a psychological disorder. 
• FUTURE RESEARCH: focused on link between swine flu vaccine, pandemic and childhood narcolepsy as there was an increase in the disorder in Finnish/Swedish children after the vaccination. 

• Campbell Et Al (2004): 56, 2 year olds. Asked to pick out specific pictures from a picture book to assess the information in their gender schema. At 2: half the children could pick out the same sex child; basic gender schema but couldn't do tasks showing that their schema had information about toys/games for their group. At 3: half had schemas with information about toys/games for their in group; SUPPORTS as it shows schemas rapidly become complex. 
• Hill & Flom (2006): measured how long 2 year old children looked at male/females performing stereotypical behaviour (male/female shaving, male/female applying lipstick) the children looked longer at gender inconsisten activities as it didnt match their schemas; SUPPORTS that by 2 years old, the children had developed schemas. 
• Bandura (1992): 4 year olds said they felt good about playing with gender appropriate toys and bad when playing with gender inappropriate toys; SUPPORTS as they have schemas about whats appropriate; Kohlberg said this would happen later.
• Tenebaum & Leaper (2002): similarity between parents schemas and their child's view about gender; gender schema theory doesn't consider where they come from. 

• Gender schema theory by Martin & Halverson (1981) agrees with Kohlberg that gender roles are driven by cognition however argues that the process of gender development starts much earlier from even the age of 2. 
• Behaviour is driven by schemas = a basic set of knowledge of gender appropriate behaviour. 
• When the child knows it's gender, they focus on their gender, in in-group and ignore information about the out-group e.g. a boy would consider male information to belong to males and gender inconsistent information as beloning to females. 
• Adolescents have more flexible gender schemas as they understand that gender roles are socially constructed and they become less sex-typed and more androgynous. 

• LOW SCIENTIFIC: as it's hard to measure objectively, not accurate to measure a psychological explanation. 
• DETERMINSTIC: inflexibility of gender schemas so children have little choice in choosing what gender they will end up as, with them being strongly influenced by processes of socialisation that are out of their control.
• NATURE IGNORED: effects of genes/ hormones aren't considered but its proven that differences such as chromosomes affect gender/ 
• HOLISTIC: although inclusion of SLT means that multiple perspectives are considered, it remains REDUCTIONIST due to the way that individual differences, psychodynamincs/biology is ignored. 
• GENDER BIAS: males are more likely to be punished for behaviour that deviates from gender norms than females. 
• FEMINSIM: removal of housewives in the 60's, girls can choose own role in family but males are still restricted.