It would seem that it is the increased levels of stress hormones, leading to a constant state of arousal which potentially causes insomnia. This was demonstrated by Vgantgas who found that primary insomniacs have increased levels of the hormones ACTH and cortisol. This is supported by Winkelman who found that primary insomniacs studied over six months had less GABA. Both these studies suggest that, due to the abnormal levels of stress hormones primary insomniacs may have they experience constant levels of arousal and therefore they cannot sufficiently reduce their brain activity to the degree of relaxation that is necessary for sleep to occur. This convergent evidence lends considerable support to the idea that primary insomnia is potentially caused by hyper arousal and insufficient levels of G.A.B.A to monitor this arousal.
A strength of this study is it’s use of objective measures; they studied the levels of biological hormones and neurotransmitters which could not possibly have been affected by the person conducting the research meaning that the experimenters can ascertain that it is in fact the relationship between primary insomnia and arousal that they are studying. This use of scientific objective measures means it is possible to establish a strong cause and effect relationship between the two variables- this means the research has more scientific value and is more likely to be accepted by the wider scientific community which could lead to increased funding for this field of research. This in turn leads to a furthered understanding of primary insomnia and it’s causes which could lead to effective treatments developed for primary insomnia which would alleviate the suffering of many insomniacs and could dramatically improve their quality of life.
There seems to be much evidence that there is a genetic predisposition to study from insomnia and the closer the relationship, the more likely those family members will suffer insomnia. For example Watson et al found MZ twins have higher concordance rates than for DZ twins, this suggests that a genetic component is involved. If insomnia was caused by environment both types of twins would have similar concordance rates but as the genetically identical MZ twins have higher levels of concordance it seems that it is more ones genetic make-up than the environment you live in that may cause insomnia. However the concordance rate is not 100%, suggesting that the cause of insomnia is not purely genetic- there must be other factors involved.
This research is supported by a study by Battea- Bonneau who found that 35% of insomniacs had a 1st degree relative with insomnia, 20% of these were mothers and 11% sisters; fathers and brothers had far lower concordance rates. These convergent findings lend considerable support to the idea that insomnia has some sort of genetic root. It could be argued that insomnia runs in close families merely because they live together, and if one family member is often stressed and aroused the others are also more likely to experience high levels of arousal, a potential cause of insomnia. However the fact that concordance rates for insomnia are higher among female relatives suggest that there is in fact a genetic component involved; surely if insomnia was caused by environment there would be an equal number of boys and girls in families suffering from insomnia. However as insomnia seems to be passed on from female to female more often, it seems reasonable to suggest that insomnia could be caused by some gene more dominant in women than in men. However suffering from primary insomnia is associated with neurotic personality types- a personality factor more common among women than among men which could explain the heightened concordance rates in women. If insomnia is genetically inherited then there is very little that can be done about it, however if it is caused by the environment people are brought up in…
An exact gene for insomnia has not been discovered in humans which rather detracts scientific weight from the explanation- however Joho et al found that mice displaying behaviour similar to human insomnia had a mutation in the gene that controlled electrical excitability in the area of the brain which controlled slow wave sleep; this part of the brain became overactive and the mice found it impossible to stay in slow wave sleep for long periods of time. If this is the case for humans and insomniacs also have some sort of genetic mutation…
However to consider any one of these explanations in isolation is reductionist: to merely consider the role of stress hormones is biologically reductionist and to consider personality type as the only explanation for insomnia is an example of machine reductionism for example. By doing this we risk hindering our understanding of the causes of insomnia; by narrowing the potential cause down to one factor we can learn in great depth the role of G.A.B.A in insomnia for example but we ignore other potential causes such as a gene that makes insomnia more likely. By doing this we could create a completely false picture of the causes of insomnia- it would be surely more constructive to use an interactionalist approach which studies all explanations and the way they link together, for example the way that certain personality types could have higher levels of arousal, in order to create a fuller picture of the causes of primary insomnia.
by
niloofer (student)
