![]() ![]() One of the phenomena triggering it is the dysregulated hypothalamic-pituitary-adrenal axis, which affects the nervous system and hormones. Insomnia has multiple causes, and its health outcomes are also varied. Altogether, insomnia may be caused by trauma and induce other mental conditions. Insomnia increases the risk of anxiety, depression, psychosis, and alcohol abuse, with the first two being particularly prominent outcomes (Hertenstein et al., 2018). However, even if comorbidity does not develop initially, the latter will still serve as a foundation for other mental disorders (Hertenstein et al., 2018). Whether the traumatic event happened as a result of the patient’s actions or beyond their control also matters: the former is more likely to provoke guilt and shame, which increases insomnia’s likelihood (Hertenstein et al., 2018). For instance, an insomniac person is unlikely to have post-traumatic stress disorder beforehand moreover, such a trait as sleep reactivity makes one more susceptible to insomnia than other outcomes (Hertenstein et al., 2018). As a result, people develop certain conditions, varying from insomnia to depression, and their occurrence depends on many factors (Hertenstein et al., 2018). The traumatizing experience may occur in one’s childhood or adulthood: they differ in rapid eye movement fragmentation, with the former causing its increased form (Hertenstein et al., 2018). Insomnia manifests as a response to trauma, which makes it related to other mental disorders. Overall, insomnia can be a genetic condition and entail type 2 diabetes, although the connection requires further studies. Genetically, insomnia tends to be linked with similar mental conditions but may also result in such a physical health outcome as diabetes because a correlation exists between it and sleep duration (Lind & Gehrman, 2016). The disorder’s inheritable nature is also evident due to its occurrence in children, who are less susceptible to other common stressors (Lind & Gehrman, 2016). Their role is to cause hyperarousal through wake-promoting neurons, which prompts insomnia (Lind & Gehrman, 2016). Both serotonin and dopamine transporters are subject to genetic studies, and their association with insomnia continues to be supplied with more evidence (Lind & Gehrman, 2016). Although examining twins contributed significantly to proving insomnia’s heritability, determining the exact genes responsible for its development remains challenging due to phenotype inconsistencies (Lind & Gehrman, 2016). ![]() They indicate that the disorder is inheritable to a moderate degree, while the female population is more likely to be affected (Lind & Gehrman, 2016). Thus, insomnia is a result of the dysregulated hypothalamic-pituitary-adrenal axis and, in turn, induces heart conditions with severe effects on one’s well-being, although a cardiovascular disease may also trigger insomnia.Īnother prominent cause of insomnia is rooted in genetics, which has been established through family and twin studies. On the other hand, HF is one of insomnia’s causes, which creates a cycle when one cardiovascular disease leads to insomnia, and it subsequently increases the incidence risk of similar outcomes (Javeheri & Redline, 2017). They are mostly responsible for mortality cases in insomniac patients as the disorder itself is not lethal, but its consequences may endanger one’s life (Javeheri & Redline, 2017). ![]() The latter is directly associated with such cardiovascular conditions as hypertension, heart failure (HF), and coronary heart disease (Javeheri & Redline, 2017). As a result, a person begins experiencing insomnia, which can manifest as a short sleep duration (Javeheri & Redline, 2017). The consequences include the elevated activity of the sympathetic nervous system and hormonal imbalance (Javeheri & Redline, 2017). For instance, the hypothalamic-pituitary-adrenal axis is said to cause the disorder if it experiences dysregulations (Javeheri & Redline, 2017). Insomnia can have many precursors, some of which will lead to other conditions. ![]()
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