Explanations of Insomnia

Primary insomnia can be learnt through association after experiencing stress-related insomnia. When insomnia occurs that is a result of stress and anxiety, an association forms between the bed and sleeplessness, so insomnia persists even when stress disappears. Sleep-related anxiety and the expectation of insomnia leads to learned insomnia, in a self-fulfilling prophecy.

This explanation of insomnia has found valuable real-world application in the use of CBT (cognitive behavioural therapy) to treat primary insomnia - breaking the association between the bed and sleeplessness to reduce anxiety over being unable to sleep. The success of this therapy supports the learnt explanation of insomnia - if the disorder can be unlearned through therapy, this suggests that it was a learnt behaviour in the first place.

Research by Storms and Nisbett supports the hypothesis of learned insomnia. In a clinical trial of insomniacs, participants went to sleep faster on placebo pills they believed to be stimulants, attributing their state of wakefulness to the pill rather than insomnia, so they relaxed enough to go to sleep. The group given pills they believed to be anxiolytics took even longer to get to sleep than normal, assuming that their insomnia was unusually severe that night due to their unaltered level of wakefulness. This supports the suggestion of self-generated anxiety over insomnia being a causal factor in the perpetuation of insomnia.


Gender differences in the diagnosis of primary and secondary insomnia suggests that this theory may be beta gender biased in its explanation of insomnia. The incidence rate of insomnia is higher in females, who also tend to have higher levels of anxiety and neuroticism - this supports the concept of stress as a factor which can lead to learned insomnia, but suggests that it is inaccurate to attribute the same cause to both sexes, as they experience the condition differently, with females more prone to stress-induced insomnia. It would be gender biased to assume that insomnia has the same causes in both males and females.

The genetic explanation of insomnia explains the condition as a result of an inherited gene defect in the genes responsible for the healthy function of the brain stem, leading to irregularities with the sleep/wake cycle. This is based on the observation that insomnia starts early on in life in most sufferers, suggesting that an innate biological cause rather than a learned behaviour is responsible.

Research by Watson et al supports the role of genes in the development of insomnia, studying 1800 pairs of twins. The concordance rate in genetically identical, monozygotic twins was 47%, while the concordance rate in non-identical, dizygotic twins was only 15%. This increased concordance rate in monozygotic twins supports the concept of a genetic basis for insomnia, but shows that genetics cannot completely explain the condition - monozygotic twins are completely genetically identical, so if the condition was entirely genetic in origin, they would show a 100% concordance rate. 

Although Watson et al's observed concordance rates would support the role of nature in the development of insomnia, twin studies alone are not enough to separate the influences of nature and nurture when determining a condition's origin. Monozygotic twins tend to be treated more similarly and share more similar environments than dizygotic twins, meaning that the higher concordance rate may be due to monozygotic twins sharing more environmental factors that could lead to the development of insomnia, such as stress, sleep deprivation and obesity. The concordance rates of obesity were markedly high between both types of twin - it is possible that the increased concordance rate of insomnia in monozygotic twins was a result of an increased concordance rate of obesity, a factor known to contribute to insomnia. 

Dauviliers and Tafti found further supporting evidence for the genetic explanation of insomnia, identifying several gene mutations implicated in the disorder. They also pointed to the genetic illness fatal familial insomnia as supporting evidence - an incredibly rare and heritable prion disease presenting in middle age which leads to a gradual death from sleep deprivation. The heritable nature of this disease suggests that some forms of insomnia have a definite genetic basis.

Explanations of Narcolepsy

The main explanations for narcolepsy involve genes and the neurotransmitter orexin. It has been suggested that a defective gene on chromosome 6 is responsible for narcolepsy in humans, based on the identification of a defective gene on chromosome 12 responsible for narcolepsy in dogs. These genes code for proteins in the brain which act as receptors for orexin, which plays a role in the regulation of appetite, sleep and wakefulness. With these receptors functioning abnormally, regular orexin transmission cannot happen in the brain so it cannot properly control sleep behaviour - leading to the symptoms of narcolepsy such as excessive daytime sleepiness, cataplexy and sleep paralysis.

It is also suggested that narcoleptics transition straight into REM sleep from wakefulness rather than going through light sleep and slow wave sleep first, leading to the sudden loss of muscle tone in cataplexy and sleep paralysis; hypnogogic hallucinations represent dreams experienced in a state of semi-wakefulness.

Lin et al provided supporting evidence for the role of genetics in the development of narcolepsy. Using genetic analysis techniques, a gene mutation on the 12th chromosome was identified in dogs as being responsible for narcolepsy - on a gene which regulates orexin receptors. A similar mutation on the 6th chromosome was identified on a gene with the same regulatory purposes - these results would support the hypothesis that genetics and impaired orexin receptors may play a causal role in narcolepsy. 

Thannickal et al carried out research supportive of Lin's suggested role of orexin in narcolepsy. Scanning the brains of narcoleptics and healthy controls, they found a severely reduced quantity of orexin-producing cells in the narcoleptics compared to the control group - supporting the hypothesis of abnormally low orexin levels causing narcolepsy. However, determining the direction of cause and effect is a difficulty with these results - although the reduced density of orexin cells may have caused narcolepsy, the condition itself may have caused the reduction in orexin. Causation cannot be determined, weakening the validity of the supporting evidence.

However, research by Gordon et al supports a different explanation - of narcolepsy as an autoimmune disorder, rather than it being caused by genetics or orexin. Mice were injected with antibodies from the blood of either narcoleptics or non-narcoleptics - the group injected with narcoleptic antibodies developed the symptoms of narcolepsy. This suggests that narcolepsy is caused by our own antibodies malfunctioning and attacking brain tissue, challenging the genetic and orexin hypothesis.

On one level, Gordon's research can be seen as scientifically credible through its use of a control group. The use of one group injected with non-narcoleptic antibodies to compare the experimental group to allows cause and effect to be determined - we can be fairly sure that the injection of the antibodies led to the development of narcoleptic symptoms in the mice. However, the use of non-human animals is an issue here - neurological or immune differences between mice and humans may mean that it would be overly anthropomorphic and invalid to generalise the conclusions of this study to humans - narcolepsy may not work the same way in both species.

The orexin explanation of narcolepsy has valuable real world application in the use of stimulants such as Ritalin and Modafinil to treat the excessive sleepiness associated with the condition. These stimulants act as orexin agonists, and have had much success in treating the sleepiness, cataplexy and lapses into daytime sleep that the condition causes, and the success suggests that narcolepsy does have a cause related to orexin deficiencies. 

The identification of a possible chromosome mutation responsible for narcolepsy does not necessarily mean that genes are a definite cause, as it is possible that environmental triggers can play a role. It is more likely that the condition can be explained through a diathesis-stress hypothesis, with a genetic basis requiring specific environmental stressors to be present in order to result in the condition, an interaction between the effects of both nature and nurture. Not all people with the 6th chromosomal mutation on the specific gene develop narcolepsy, while not all narcoleptics have this gene mutation - suggesting factors other than genetics are involved. It would be too reductionist to simplify the condition down to the presence of one gene, ruling out environmental triggers such as stress or sleep deprivation or biological factors such as autoimmune malfunction.

Explanations of Sleepwalking

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Sleepwalking tends to run in families, being 10 times more likely if a first-degree relative has a history of sleepwalking, and having higher concordance rates between monozygotic (genetically identical) than dizygotic (non-identical) twins. This has led to the development of a genetic explanation which suggests that sleepwalking has a genetic basis, being coded for by the presence of a certain gene.

Bassetti provided supporting evidence for the genetic explanation of sleepwalking, gene-testing 16 adult sleepwalkers to find that 50% had a gene found in only 25% of the general population - HLA-DQB1*05, partially responsible for producing HLA immune regulation proteins. The fact that HLA-DQB1*05 gene is twice as common in sleepwalkers as in non-sleepwalkers suggests that it in some way leads to the inhibition of motor control which causes sleepwalking, supporting the genetic hypothesis. However, other factors must be involved in sleepwalking, or else the gene would be present in 100% of sleepwalkers.

Lecendreux et al provide further supporting evidence for the genetic explanation of sleepwalking, finding a concordance rate of 50% in monozygotic twins compared to 17% concordance in dizygotic twins. This supports a genetic basis but not a complete explanation - it cannot be entirely genetic, or else a 100% monozygotic concordance rate would have been found.

Although the genetic explanation is well supported by research evidence, it is an overly reductionist explanation of sleepwalking, being unable to explain the condition's incidence in all sufferers. To reduce a complex syndrome down to the presence of a single gene is an oversimplification - other factors must be important, as only 50% of sleepwalkers have the gene suggested as an explanation, and there is not 100% concordance between monozygotic twins. There is research to support the role for personality factors in sleepwalking - such as Type A personalities being more likely to experience the condition - and the genetic explanation ignores these suggested personality and environmental factors and cannot fully explain sleepwalking as a result.

Additionally, the genetic explanation is overly deterministic, stating that if you possess a certain gene or combination of genes, you'll sleepwalk, while this is not necessarily the case, as 24% of people with the HLC-DQB1*05 gene do not sleepwalk. The existence of these counterexamples suggests that having the gene will not necessarily lead to sleepwalking, challenging the explanation's predictive validity. Cases of crimes comitted while sleepwalking have raised the free will versus determinism debate - in the case of Ken Parkes, who killed his family members while sleepwalking and was later acquitted for murder, the law fell on the side of determinism, claiming that he was not in control of his actions and therefore should not be held responsible.

Identical twins tend to share a very similar environment during childhood and adolescence, so the influence of nature can't be separated from the influence of nurture to determine a direct cause and effect for the genetic basis of sleepwalking. Genetically identical twins may also have shared environmental factors during upbringing such as stress, alcohol and other drug usage and sleep deprivation - due to these multiple confounding variables as aspects of nuture, sleepwalking cannot be pinned down as a result of nature through the use of concordance studies.

The psychodynamic approach explains sleepwalking as a result of repressed unconscious desires to sleep where they slept as a child, and a way of working through unconscious anxieties. During REM sleep the person is paralysed and cannot act out their dreams - once they transition to NREM and can move, this instinctive energy and desire to return to where they slept as a child is expressed through sleepwalking.

However, this explanation lacks face validity - most sleepwalkers are children rather than adults, so a desire to return to the place of childhood sleep would only explain the condition in the small proportion of sufferers that are adults. Similarly, it fails to explain the range of activities carried out by sleepwalkers - cooking food, eating - behaviours completely unrelated to returning to the place of childhood sleep. 

The higher incidence rate of sleepwalking in children than in adults is likely to be explained by the fact that children spend more time in slow wave sleep, when sleepwalking takes place - so there is more opportunity for the behaviour to occur. Also, it could be explained by parts of the brain that inhibit movement in sleep not being fully developed in children - as supported by Hublin et al who found that 20% of children experience sleepwalking compared to 2 % of adults, suggesting that a lack of neurological maturation and development is the cause. 

The psychodynamic explanation is also unfalsifiable and untestable, as the unconscious mind cannot be directly accessed reliably and objectively. The explanation does not treat psychology using the scientific methodology and objectivity that it should, and lacks scientific credibility as a result; unlike the genetic approach which uses quantifiable techniques such as genome sequencing and chromosome analysis to gather objective data.

Cultural Influences on Gender Roles

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Across the many global cultures, there are many similarities and differences between gender roles - the attitudes, behaviours and traits adopted by either sex.  Division of labour between genders is a practice found in most cultures - in the majority of societies, food preparation and child raising are primarily done by women, whereas hunting and resource provision are usually done by men. Similarly, socialisation of genders towards certain traits appears to be consistent across cultures - men are usually socialised towards assertiveness and independence; women towards assertiveness and independence. This suggests that biological factors are more important than cultural factors in determining gender roles.

However, significant differences in gender roles exist between cultures as a result of differing cultural influences. Male superiority in spatial perceptual tasks are only found in tight-knit, sedentary, and is absent or inverted in looser, nomadic societies - Berry et al suggested that these sex differences are a result of sociocultural factors rather than human biology, and suggested that conformity differences are similar in origin - a result of social environment rather than nature, being more pronounced in tight-knit, sedentary societies. This suggests that sex differences in both conformity and spatial perception are due to cultural factors rather than human biology.

Perception of "gender" also varies between cultures, with not all cultures having the binary male/female categorisation typical of the western world. The concept of binary gender categorisation not being a global norm is supported by the example of the "berdache" in Native American tribal Crow culture is a biological male who chooses to be the "wife" of a warrior rather than a warrior, but is not scorned or ridiculed for this. 

Similarities in gender roles between cultures would suggest a natural, genetic and biological component to gender roles, differences would suggest that gender roles are mainly due to nurture, environment and different socialisation processes.

Early research by Mead supports the concept of cultural differences leading to different gender roles. Social groups in the tribes of Papua New Guinea were studied; Mead found that Arapesh men and women were gentle, responsive and cooperative, Mundugamor men and women were violent and aggressive, but Tchambuli showed distinct gender roles - men were emotionally dependent, whereas women were dominant and impersonal. The presence of distinct gender roles in one tribe but not the others suggests that gender differences are a product of society and culture, rather than biology - suggesting that cultural influences are more important than biology in determining gender roles.

Mead's interpretations of her results with respect to gender roles were originally ones of cultural determinism, suggesting that differences between males and females such are a result of social rather biological factors. However, she then changed this view to one of cultural relativism, suggesting that in all three societies, men were more aggressive than women, but these differences were just expressed differently depending on cultural socialisation processes.

Williams and Best provided supporting evidence for cultural similarities in gender stereotyping, suggesting that gender roles are biological and innate rather than a result of socialisation. 2800 participants across 30 different countries categorised adjectives as either "male" or "female" in very similar ways - "dominant" and "aggressive" were almost universally categorised as male, whereas "nurturant" and "deferent" were almost universally categorised as female.


However, several methodological flaws limit the validity of Williams and Best's research. First, the adjectival allocation task was a forced, binary choice - there was no option for "neither" or "both" - the division between male and female stereotypes may have been exaggerated. Secondly, the task related to opinion stereotypes and not behaviour - although gender stereotypes may significantly affect behaviour, this is not demonstrated or measured by the study. Finally, the participants, although from a range of cultures, were all university students - this may be reflected in their values systems, being exposed to similar global influences such as books, films, and higher education. This might explain the apparent high level of cultural similarity of gender stereotyping. 

Whiting and Edwards researched the gender attitudes and behaviours of a variety of global cultures, and found that it was fairly universal for girls to be encouraged into domestic and child-rearing roles, while boys were assigned tasks involving responsibility outside the home such as looking after animals. This suggests that the concept of specific male and female gender roles is highly prevalent cross-culturally, and therefore probably biological in origin, suggesting that biological factors are more important than cultural influence in the development of gender roles.

Much of the evidence for cultural similarities and differences in gender roles comes from studies carried out by western researchers investigating both western and non-western cultures. Research methods such as Williams and Best's adjectival allocation questionnaire to measure cultural gender stereotyping were developed in western cultural contexts and may not be applicable to other cultures' behavioural norms and attitudes - it would be imposing an etic to generalise the results of these questionnaires when used in cultures other than the one they were designed in. Berry et al suggested that most cross-cultural studies carried out by western researchers reflect a western interpretation of human mind and behaviour and view participants from other cultures through this lens - they suggest the use of more indigenous researchers to reduce this bias. 

Evidence that indicates clear cultural differences in gender roles, such as that of Mead and the differences in aggression between men and women in Papuan tribes, supports the nurture side of the nature vs nurture debate, suggesting that gender differences arise due to the influence of culture in the socialisation process. Evidence that indicates cultural similarities in gender roles, such as that of Whiting and Edwards and Williams and best supports nature's influence in gender roles, suggesting that gender roles have evolved to become part of our genetic code due to serving an adaptive evolutionary purpose. Evidence supports both sides of the debate - it is ultimately likely that gender roles are a combination of both genetic factors and socialisation, interactionalist mechanisms between nature and nurture as suggested by the biological approach.

Gender Schema Theory

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Suggested by Martin and Halverson, this is a similar cognitive theory to Kohlberg's theory, emphasising the active role of the child and their thinking in their gender development. However, it differs from Kohlberg's in claiming that basic gender identity is enough for a child to actively seek to observe and imitate gender-appropriate behaviour (Kohlberg had suggested that this only happens at the gender constancy phase, around age 7) , and suggesting that the development of schemas affects later behaviour, especially in terms of memory and selective attention.


GST suggests that gender develops through the formation of schemas - mental clusters of related items which together represent a concept relating to the world. Children learn schemas from information received from their parents, other children, and media such as books and television. This leads to the development of a schema of gender-appropriate behaviour - what toys to play with, what to wear, how to act and so on. Through identifying as a boy or a girl, children join an ingroup, leading them to positively evaluate their own group, and negatively evaluate outgroups (the other sex.) This motivates the child to be like their own group and to avoid the behaviour of the opposite sex, and actively seek information about their ingroup's behaviour, acquiring an ingroup schema.


This leads to the resilience of gender beliefs, where the child holds firm and rigid schemas that are resistant to change, influencing selective attention. They will ignore or misremember information that conflicts with their schemas - for example, if a boy sees a film with a male nurse, the existing schema is not altered - this schematic anomaly is ignored.


Supporting evidence for the early formation of schemas as an aspect of GST comes from a study by Campbell (2000.) A visual preference technique was used to observe babies aged 3, 9 and 18 months, finding in both sexes a preference for observing same-sex babies (more noticeable in boys) - with both genders preferring to watch "male" activities. This supports Martin and Halverson's suggestion that babies develop schemas long before they are able to speak, and that schemas drive selective attention - supporting GST's central tenet of gender ingroup formation leading to selective attention to same-sex ingroup members exhibiting gendered behaviour.


Further supporting evidence for GST comes from Poulin-Dubois et al, who asked 63 Canadian toddlers to choose a doll to carry out a series of tasks typically thought male, female or neutral. Girls aged 24 months chose the "gender-appropriate" doll, which boys did not do until 31 months. This is concordant with Cambell's findings that young children pay selective attention on a sex basis between the age of 24 and 31, far before Kohlberg's suggested age of 7 years.


However, both of these studies found gender differences between boys and girls - in Campbell's study, boys preferred to watch same-sex activities, whereas girls preferred to watch opposite-sex activities; in Poulin-Dubois et al's study, girls and boys developed the ability to identify gendered behaviour at different ages. GST claims that boys and girls develop their gender identity in the same way, so it cannot account for these differences. It would be beta bias to generalise the same developmental mechanisms to both genders, as research evidence suggests that girls and boys develop their schemas in different ways at different times.


Tenenbaum and Leaper criticised GST, claiming that it doesn't explain where schemas originate from, only their role - despite the importance of schemas - and sought to explain this aspect of GST. Carrying out a meta-analysis of 43 studies involving 10'000 participants, they looked for a relationship between the gender schemas of parents, and those of their children. They found an overall correlation of +0.16 - weak, but significant. This indicates that gender schemas are partially learnt through socialisation by parents - this correlation was too significant to be explained by chance.


Tenenbaum and Leaper's research can be considered culturally biased, taking place in predominantly Western and industrialised countries such as North America and Europe, with only 1 of 43 taking place in Asia. Bearing in mind how much parenting practices differ between cultures, it's imposing an etic to suggest that inheriting schemas from parents through socialisation is a global developmental norm - other cultures may place less emphasis as European cultures do on children growing up to be a reflection of their parents' beliefs and values.


GST helps us understand why children's beliefs and attitudes about gender roles and behaviours are so inflexible - children only pay selective attention to information that is consistent with or confirms their schemas.  Therefore, if children see someone engaging in a schema-inconsistent behaviour they'll ignore or forget it.


Compared to the biological approach, this theory heavily supports the role of nurture, suggesting gender is learnt through ingroup schemas and observation/imitation of the same sex; the biological approach supports natural factors such as the influence of hormones, chromosomes and neuroanatomy as being the most important factors in gender development. Both theories have research to support them - with evidence such as the David Reimer case study supporting the role of genetics, and Campbell et al's visual preference technique supporting the role of selective attention. There is evidence for both sides of the debate, leading to the increasing popularity of the interactionalist biosocial approach, suggesting that gender is a result of both biology and environment.


This approach is based around social learning from members of same-sex ingroups, suggesting that we learn gender appropriate behaviour through the socialisation process. Kohlberg's cognitive developmental approach suggests a similar method - we pass through developmental phases of how we understand gender, but only at the stage of gender constancy experienced after the age of 7, do we pay selective attention to gendered behaviour. Although the approaches are similar, they differ strongly in this key factor, with Martin and Halverson suggesting that we have the cognitive ability to observe and imitate gendered behaviour from between two and three years old.

Social Influences on Gender

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Gender roles are learned through observation and imitation of live and symbolic models - for example, parents, teachers, peers and the media, who convey social messages about the importance of gender role-appropriate behaviour. We observe their examples of gender-appropriate behaviour and then seek to imitate them in the social learning process. Based on learning theory principles of operant conditioning, children are seen as being positively reinforced for behaving in gender-appropriate ways.

Socialising agents model examples of appropriate and inappropriate behaviour, and also the consequences of conforming or not conforming to gender norms.

Through observational learning, children acquire knowledge regarding gender roles without actually ‘doing’ anything; children observe gender role models being reinforced or punished for gender-appropriate and gender-inappropriate behaviour (vicarious reinforcement) and will imitate behaviours that they saw being reinforced and not imitate those they saw being punished. SLT therefore explains the acquisition of gender role stereotypes in this manner.

Gender appropriate behaviour is reinforced by parents giving praise and toys. Fathers have been shown to reinforce gender-appropriate behaviour more than mothers (especially in sons)

Supporting evidence comes from Lytton & Romney (1991), who found that parents reinforced with praise and attention stereotypical gender behaviours in both boys and girls – for example, what activities they participated in – suggesting that social environmental factors are important in determining gender behaviour. However, children were also raised similarly in many ways, suggesting that reinforcement alone cannot account for the development of gender behaviours.

Further supporting evidence comes from Fagot & Leinbach (1995), who compared children raised in ‘traditional’ families, where dad went to work and mum cared for children, with children raised in ‘alternative’ families, where mum and dad shared child care. At age 4, children were given gender-labelling tasks as a means of testing gender schemas. The ‘traditional’ family children displayed more gender role stereotyping and use gender labels earlier, suggesting that parents do act as gender role models for their children.

TV, cinemas, magazines, music play a role in the acquisition, shaping and maintenance of gender roles. Males tend to be more represented on TV and tend to be in higher-status roles. Males and females portrayed in gender stereotypical ways. Media is invasive and persistent.

Supporting evidence for the role of the media comes from Pierce (1993) who conducted a content analysis of teenage girls’ magazines. Girls tended to be portrayed as weak and reliant on others, with a focus on being in a relationship rather than having independent aspirations, demonstrating the influence of the media in establishing gender attitudes and behaviours, and supporting social learning theory’s explanation.

Peers have a strong influence, especially when children are slightly older. Children show preferences for same-gender playmates and segregate into same-sex groups. Peers are intolerant of gender-inappropriate behaviour, regulating one another! Young children’s gender role stereotypes are very rigid, but become less so as children mature.

Supporting the influence of peers in gender development, Archer & Lloyd reported that 3-year-old children who played the opposite sex’s games were ridiculed by their peers and ostracised, supporting the idea that peers police gender roles. This supports the idea that children develop an idea of what constitutes gender-appropriate behaviour from how their peers react to behaviour, supporting the role of peers in the social learning process.

Challenging the idea that gendered behaviour is directly learnt from peers, Lamb & Roopnarine observed preschool children at play and found that when male-type behaviour was reinforced in girls the behaviour continued for a shorter time than when male-type behaviour was reinforced in boys. This suggests that peer reinforcement mainly acts as a reminder, rather than as a way of learning gender appropriate behaviour – the children had already learnt the behaviours from their parents.

Compared to other explanations such as the evolutionary and the biological approaches, theories of social influences on gender fall firmly on the nurture side of the nature-nurture debate, explaining gendered behaviour as a direct result of learning processes – mainly through social learning from parents, peers and the media. This sharply opposes the biological approach, for example, which claims that gender development results from the influences of hormones, genetics and neuroanatomy – strongly backing the role of nature in the debate. Both explanations have significant research evidence to support them – for example, the case study of David Reimer for the biological approach, the research of Lytton and Romney for the influence of society. This has led to the increasing popularity of the interactionalist biosocial approach, which explains gender development as an interaction between environmental and biological processes.

Theories of social influence are primarily based around the learning approach, ignoring other factors such as cognitions (as suggested by Kohlberg’s cognitive developmental approach), neuroanatomy and behaviour-influencing hormones such as testosterone (as suggested by the biological approach) and genetics over the course of our evolutionary history (as suggested by the evolutionary approach.) With a significant level of research support, social influence theory can be considered strong in its own right, but fails to account for many other factors shown to affect gender, being reductionist in its attempt to simplify such a complex area such as gender development into the result of simple behavioural learning processes.

Research into the effects of social influence on gender has important real-world application in challenging certain regressive or outdated gender stereotypes in society – changing social norms and expectations through the portrayal of non-traditional gender stereotypes in the media. For example, Pingree (1978) found that stereotyping was reduced when children were shown advertisements with women in non-traditional gender roles, leading to pressure on programme makers to use this information to challenge attitudes. However, not all research supports the effectiveness of this technique – Pingree found that pre-adolescent boys experienced stronger stereotypes after being presented with examples of non-traditional gender roles, perhaps a backlash which occurs due to boys of this age wanting to take a view counter to that of views held by adults. Similarly, this conflicts with gender schema theory’s suggestion that information inconsistent with our rigid gender schemas is misremembered or ignored.

Biosocial Theories of Gender Development

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The biosocial approach takes a social constructionist approach to gender development. arguing that concepts of gender are artificial and a result of social norms rather than being an innate biological concept.


Money and Ehrhardt's biosocial theory suggests that gender development is the result of interactions between biological and sociocultural factors. Biological factors include chromosomes (XX for a female, XY for a male), and the neurodevelopmental and physical effects of prenatal hormones such as testosterone. Sociocultural factors include early socialisation based on cultural responses to biological stereotyping - this stereotyping can include the labelling of a child as a boy or a girl by parents and peers. The biological factors that lead to parental labelling as "girl" or "boy" then lead to different environments and reactions from others, which lead to gender development as boys and girls are socialised in different ways - leading to gender role identity and sexual orientation.


Eagly and Wood's social role theory suggests that psychological gender differences are a result of roles which men and women are assigned, which were a result of physical differences in our evolutionary history. For example, in our history, men were assigned the role of hunter due to their larger size - this lead to psychological, gendered characteristics such as aggression and impulsivity. Females were assigned the role of homemakers, which lead to psychological, gendered characteristics such as being empathetic and nurturing. While evolutionary theory states that selection pressures lead to physical and psychological differences which determine gender roles, social role theory suggests that physical differences lead to differently assigned gender roles, which lead to psychological differences as an aspect of gender.


Supporting evidence for the biosocial theory of gender development comes from Smith and Lloyd's 1978 study. Babies were dressed in non-gender specific clothes, then labelled with a male or female name. It was found that people would play with them in different ways according to their gender label, with boys being treated in a more physical manner. This supports biosocial theory's suggestion that initial parental gender labels (which participants believed was based on biology) affect how the child is treated and the socialisation process, providing evidence for the hypothesis that biological labels lead to different environments and social interactions, influencing gender development.


Schaffer (2004) provides further supporting evidence for the biosocial theory. A sample of 200 adults was showed a video of a 9-month-old baby, named "David" or "Dana", playing with toys and responding to stimuli. The adult labelled the baby's behaviour and emotions in gender typical ways according to whether they believed it male or female. Again, this shows that the gender identity label affects how others in society react to and stereotype the child, causing different gender development. This supports the biosocial hypothesis that biological labels as "male" or "female" lead to differential treatment from society, leading to different socialisation processes and gender development.


However, conflicting evidence for the biosocial approach comes from a study by Luxen (2007), finding sex differences in toy preferences in very young children even before socialisation can take place. This suggests that innate gender differences exist before the socialisation process - implying that gender differences are a result of pure biology rather than a reaction between biology and social environment. This challenges the approach's claim that gender role and identity is a result of socialisation based on biological sex, suggesting that nature is far more important than nurture.


The case study of David Reimer provides further conflicting evidence for the biosocial approach to gender development. Regardless of the way his parents attempted to socialise him to be psychologically female, adopting feminine traits and gender roles, upon learning his true genetic sex he rejected these attempts at socialisation and began to identify as male despite opposite parental labelling. The fact that a biological male who was socialised through toys, clothes, name and social environment as female still ultimately identified as male suggests that biology is a much more powerful force than society is in gender development, challenging the biosocial approach's claim of biological and social interactions being responsible.


The biosocial approach theoretically combines both biological and environmental factors to explain gender development, and could therefore be considered more holistic than approaches such as the evolutionary or cognitive-developmental approaches, which explain development in terms of either biology or thought processes, not both. This approach does not reduce gender development to a single, exclusive account of human behaviour. However, the majority of research points to either biological or social aspects as being the determining factor in gender development - not both! For example, Luxen's research and the case study of David Reimer firmly suggests that biology is more important than environment - no studies show an equal importance of biology and society, suggesting that a holistic explanation of gender is inaccurate.


However, in contrast to other theories such as the biological and evolutionary approaches and Kohlberg's cognitive developmental model, the biosocial theory does not explicitly favour either side of the nature-nurture debate. Instead, it assigns a role to elements of nature, through its biological sex component, and elements of nurture, through the importance of socialisation in the development of gendered behaviour. It is an interactionalist approach, unlike other approaches which could potentially oversimplify gender by explaining it as purely a result of neuroanatomy and genetics, or of cognitive processes, or of social learning.


Social Role Theory has an important real world application in lending scientific credibility towards egalitarian philosophies such as feminism, working to bring about a state of greater gender equality. Whilst approaches such as the evolutionary theory have been regarded as a force against gender equality, stating that sex differences are innate and cannot be changed by altering social contexts, the social role approach emphasises the flexibility of gender roles and behaviour. This gives it high ethical appeal because sex roles are perceived as a result of social and biological factors rather than purely biological, therefore more flexible, offering people opportunities to create and develop aspects of the self which may otherwise be constrained by typical ideas of masculinity and femininity.