Factors which contribute to the onset of insomnia
1. Predisposing, precipitating and perpetuating factors
A neurobiological model of insomnia, known as the Spielman model (also referred to as the 3-P model) defines predisposing, precipitating and perpetuating factors relating to insomnia. The model proposes that these factors are relevant to both the development and treatment of insomnia.
There have been many other models addressing the symptoms and various influencing factors of insomnia, a fair percentage of which focus on psychological and behavioural response patterns.
The Spielman model, is one that has been developed from clinical and basic neuroscience observations measuring activity patterns in specific regions of the brain. The model is structured in a manner which concludes that all psychological and behavioural patterns ultimately have neurobiological origins (i.e. behavioural patterns are expressions of brain region or circuit activity).
According to the model, relevant factors can be defined as follows: (6)
- Predisposing factors: These involve physiological factors, psychological diatheses (susceptibility to a specific condition) and genetic predisposition. Such factors may influence an occasional night of poor quality sleep, and not necessarily trigger insomnia.
- Precipitating factors: These include psychological stressors, as well as physiological and environmental factors that contribute to the development of acute insomnia symptoms. Such stressors or factors will arise in the form of a specific event, such as a trauma affecting a family, occupational stress or the development of a health issue. Precipitating factors are normally simple to pinpoint, either by a doctor or the person experiencing insomnia themselves.
- Perpetuating factors: These involve psychological, physiological, environmental and behavioural factors which persistently interfere with the re-establishment of normal sleep cycles. In this instance, such factors can lead to the development of chronic insomnia, even if a precipitating factor has been removed or resolved.
For example, behavioural factors can easily perpetuate persistent insomnia. Often, people struggling with ongoing insomnia attempt to compensate for sleep that is lost by changing their behavioural patterns. Many may try and make up for lost sleep by deliberately staying in bed for longer periods (whether awake or asleep), sleeping in, or taking naps during the day. This doesn’t usually achieve the desired effect and instead, fragments sleep further, worsening symptoms.
Excessive worrying is also typical of people with persistent or chronic insomnia, leading to obsessive behaviours relating to sleep. Such behaviours tend to exacerbate sleep disruptions, as well as reduce a person’s natural homeostatic drive, which impacts a normal or habitual sleeping time.
It’s not uncommon for such individuals to develop conditioned arousal to specific stimuli they would normally associate with sleep, thus stimulating anxiety about going to sleep as a result. Anxiety breeds increased agitation and ruminative thoughts at a time when a person would normally wish to be asleep.
The Spielman model is a useful analytical tool to help clinically identify problems with targeted treatment measures. It is widely agreed that this model is structured in a way that has an integrated and flexible view of insomnia, taking into appropriate consideration all relating factors.
A complex network of genes is believed to be responsible for the process of sleep, instead of just one type or even a subset of genes. Along with genes, signalling pathways and neurotransmitters also play a role in wakefulness.
Network clusters of neurons which promote sleep exist in numerous regions of the brain and become active in preparation for sleep as a person nears time for bed. These neurons function as nerve-signalling neurotransmitters (chemicals) which effectively reduce cell activity, helping to promote muscle relaxation and sedation. Genes play a role in controlling the excitability of neurons and influence circadian rhythms.
Genetic predisposition and external factors which influence sleep (such as stress, light exposure or caffeine intake) have been identified as having a direct influence on a person experiencing insomnia. In insomnia sufferers, notable changes identified in the adenosine2A receptor gene (ADORA2), appear similar to the blockage of adenosine A2A receptors experienced by individuals sensitive to caffeine. (7) This gene variation in a person with insomnia causes the individual to exhibit changes in electrical brain activity similar to those induced by caffeine intake in other individuals.
Some genes linked to insomnia include those involved in the regulation of circadian rhythms. Mutations in these genes, namely Per2, which is a member of the period family of genes responsible for metabolism, behaviour and locomotor activity, can result in circadian rhythm disorders like advanced sleep phase and delayed sleep phase syndromes.
Other genes involved include CLOCK (circadian locomotor output cycles kaput which affects the period and persistence of circadian rhythms), and the GABAA beta 3 subunit. Fluctuations and changes in serotonin receptor transporter genes also influence a person’s ability to cope with stress, sometimes resulting in a susceptibility to depression. Serotonin, a monoamine neurotransmitter, is an important component relating to arousal or wakening mechanisms.
Other chemicals in the mix, all contributing to the process of sleep and wakefulness include norepinephrine, orexin (also known as hypocretin), adrenaline, acetylcholine, histamine and cortisol.
Changes in the prion protein gene PRNP can sometimes result in a rare condition known as fatal familial insomnia (FFI) which is characterised by severe sleep disruptions which can progress to hallucinations, as well as significant motor and cognitive deficiencies and autonomic problems. Death inevitably occurs as a result.
Genetic factors are still under extensive research when it comes to the influences and causes of insomnia.
A person experiencing chronic insomnia typically displays signs of increased brain arousal or activation (often associated with heightened anxiety), with distinctive changes in daytime sleepiness, personality behaviours and metabolism levels in comparison with normal, healthy individuals.
It is common for people with chronic insomnia to experience EEG signs of hyperarousal – i.e. heightened fast-frequency electrical activity in the brain during NREM (non-rapid eye movement) sleep states. A person with the condition will also show signs of deactivation in the sleep-wake areas of the brain during NREM sleep.
Those experiencing insomnia generally also have higher than normal body temperatures during both the day and the night. Elevated levels of urinary cortisol, adrenaline secretion and ACTH (adrenocorticotropic) hormone are also present.
In this regard, physical changes to the body bring about a state of hyperarousal similar to that experienced by individuals who have just consumed caffeine. Nocturnal manifestations of hyperarousal may thus have more to do with daytime impairments and dysfunction than an actual lack of quality sleep.
6. US National Library of Medicine - National Institutes of Health. 2011. A Neurobiological Model of Insomnia: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3212043/ [Accessed 04.08.2018]
7. American Society for Clinical Pharmacology and Therapeutics. 28 February 2007. A Genetic Variation in the Adenosine A2A Receptor Gene (ADORA2A) Contributes to Individual Sensitivity to Caffeine Effects on Sleep: https://ascpt.onlinelibrary.wiley.com/doi/full/10.1038/sj.clpt.6100102 [Accessed 04.08.2018]