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

Black: AO1 - Description
Blue: AO2 - Research
Red: AO3 - Evaluative points/IDAs

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

Black: AO1 - Description
Blue: AO2 - Research
Red: AO3 - Evaluative points/IDAs

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.