Insomnia is the most prevalent sleep disorder, affecting millions of individuals worldwide, significantly impacting their quality of life and overall health.^[1] Recent studies have demonstrated that insomnia rarely occurs in isolation but rather interacts with various mental and somatic disorders. Conditions such as depression, anxiety, and cardiovascular diseases often exacerbate symptoms of insomnia, leading to a vicious cycle of poor sleep and deteriorating health.^[2] Conversely, chronic insomnia can contribute to the onset and worsening of these diseases, highlighting a critical area of concern for both patients and healthcare providers. Insomnia is defined by difficulty initiating sleep (sleep onset more than 30 minutes), inability to maintain sleep (multiple awakenings during the night), and early morning awakening (before the desired time), coupled with daytime sequelae.^[3] The described complaints are present at least 3 days per week and cannot be explained by another underlying sleep disorder. Chronic insomnia is present when the symptoms persist for at least 3 months.^[4] Chronic insomnia (CI) is the most common sleep disorder worldwide and is one of the most common complaints in general practi- ce.^[5] Data from population studies in Europe, the USA, and Australia show similar results, indicating 6% to 10% prevalence of CI as a nosological entity, and up to 35% as a symptom of disturbed sleep.^[5,6] If acute, short-term insomnia is also considered, the lifetime incidence is as high as 50%.^[1]

Insomnia, both as a symptom and as a clinical disorder, is significantly more prevalent in women, with a female-to-male ratio of 1.41.^[7] On the one hand, this correlates with a higher frequency of depressive disorders in women, while on the other, women are more likely to seek medical attention and are better diagnosed.^[8]

The demographic prevalence of insomnia increases with age. About 25% of people above 65 years of age have a chronic sleep disorder, described as insomnia, while 48% manifest it as a symptom, which however does not mean that insomnia is a natural phenomenon of ageing.^[9] A likely explanation is the increased incidence of psychiatric and organic diseases, which can serve as precipitating factors in the genesis of CI. Additionally, other sleep disorders like sleep apnea and restless legs syndrome, which may cause insomnia are much more common in the elderly.^[1] Visual impairment, especially cataract may block blue light, causing circadian rhythm disturbances, which can contribute to the development of CI.^[10]

According to the current clinical classification, insomnia is classified into three categories – chronic insomnia, lasting more than 3 months; short-term insomnia (acute, subacute), lasting less than 3 months; and other insomnia disorder.^[3] The contemporary approach does not incorporate subtypes of insomnia based on distinctive characteristics of the patient’s profile, as well as clinical and behavioral aspects. The present definition eliminates the differentiation between “primary” and “secondary” (caused by another disorder) insomnia, as there are no objective differences in the clinical course, therapeutic response, consequences, and outcome of the disorder.^[1,3,5]

Based on objectively measured parameters, alternative approach to the classification of CI provides a novel framework at the differences between individual groups of insomnia patients.^[11] Based on the total sleep duration, two phenotypes of CI have been composed: (1) Total sleep duration less than 6 hours (insomnia with short sleep duration, ISSD); (2) Total sleep duration of more than 6 hours (insomnia with normal sleep duration, INSD).

There is a marked difference between the two phenotypes in terms of comorbidities, complications and response to therapy (see Association with other diseases).

The classic model describing the occurrence, progression, and establishment of CI was proposed by Spielman and colleagues in 1987, known as the 3-P model or behavioral model for the development of insomnia.^[12] This approach recognizes three groups of factors, which (1) form the terrain for the development of the disorder, (2) play the role of a trigger mechanism, and (3) permanently consolidate the symptoms into a chronic disorder. The author named these factors “predisposing, precipitating, and perpetuating,” respectively (Fig. 1). The 3-P model describes how acute sleep impairment occurs against the background of a predisposition and the behavioral mechanisms by which the disorder becomes chronic.

The “predisposing factors” include those that make an individual’s sleep vulnerable and increase the risk of developing insomnia after a provocation. These include genetic predisposition and heredity, female sex, advanced age, certain personality traits such as neuroticism and perfectionism, or a combination of the above.

The “precipitating factors” are life events, interfering with the predisposing factors, usually leading to significant distress, which provokes initial sleep disruption and is the basis of acute insomnia. This is the broadest group and includes all causes of significant psycho-emotional stress – the death of a loved one, financial difficulties, physical and mental health disorders, substance or medication abuse, trauma, etc. If the patient manages to overcome the precipitating factor and restore their sleep structure within 3 months, then CI does not develop. However, any past acute episode increases the risk of a relapse and may appear as a predisposing factor.^[4,13]

The “perpetuating factors” play a crucial role in the establishment of CI. These are behavioral and cognitive factors that do not allow the individual to overcome the acute episode of insomnia, by feeding maladaptive behavior and are responsible for the chronification of insomnia. Perpetuating factors are ostensibly logical behavioral responses that turn out to exert perpetrating negative effects on sleep and include prolonged bed rest, daytime naps, watching movies, listening to music, etc. For example, prolonged bed rest, when the individual goes to bed too early, stays awake in bed at night, or “lays out” in the morning fosters the formation of a pathological association between bed and wakefulness, hindering passive initiation of sleep.

The main complaints are related to the persistent inability to fall asleep or maintain stable, restorative sleep (Fig. 2).^[13] Patients typically need more than 30 minutes to fall asleep, have multiple awakenings during the night, and/or wake up earlier than desired. They often report that they sleep better on the nights preceding days off or that their sleep is improved if they sleep at a new place. The latter could be related to a change in the stimuli in the bedroom that do not evoke the pathological arousal association.^[14] Cognitive hyperarousal is indicated by mental rumination, the incessant flow of thoughts, and the increasing anxiety and catastrophizing about the upcoming sleepless night.^[15] They are the basis for the inability to initiate sleep passively. Additionally, data can also be found on physiological arousal – palpitations, increased skin temperature, tendency to sweat, and restlessness in bed.^[1]

Complaints present during the day are non-specific and include reduced work capacity, lack of motivation, desire for work and activity, and weakened memory. Patients share that they are tired but rarely sleepy and attempts to nap in the afternoon are usually unsuccessful.^[1,15]

Often, patients with CI have features characteristic of anxiety-depressive spectrum disorders – mood swings, anxious thoughts, inability to experience pleasure (anhedonia), decreased libido, increased irritability, and worries about the upcoming sleepless night.^[16] The tendency to somatize complaints is typical – often symptoms such as “constant headache”, tremor, blurred vision, etc. are among those frequently reported by the patient.

Insomnia is the most common sleep disorder and the most common symptom in sleep medicine, reported by over 50% of the general population.^[3,13] Due to its high prevalence, a significant relation between CI and other diseases – somatic and psychiatric – is also expected.^[17] Insomnia can precede other disease onset, co-occur with it and influence its course, or be a consequence of a present disorder despite its adequate treatment, which implies the difficulties in creating a unified diagnostic and therapeutic approach to all cases of CI.^[18]

The interplay between chronic insomnia and mental health disorders is well-established. Polysomnographic data of disturbed sleep have been reported in almost all psychiatric disorders.^[19] Insomnia is often the initial symptom of many psychiatric disorders, most notably major depressive disorder (MDD) and generalized anxiety disorder (GAD).^[18] The relationship between CI and disorders of the anxiety-depressive spectrum and/or affective psychiatric continuum is bidirectional and multifactorial.^[17] Strong correlations have been found in the relationships between insomnia, depression, obsessive-compulsive disorder, alcohol abuse, anxiety disorders, phobic disorders, high suicide risk, etc.^[20–22]

Insomnia can often be caused or exacerbated by somatic diseases, which also act as a precipitating factor.^[11] For instance, chronic pain, malignant diseases, as well as respiratory diseases (bronchial asthma and chronic obstructive pulmonary disease) can play a role as aggravating factors in patients, prone to insomnia.^[36–38] The mechanisms through which these diseases affect sleep include changes in daytime physical activity and circadian misalignment, activation of the hypothalamic-pituitary-adrenal (HPA) axis at night, changes in neurotransmitter action in the CNS, promoting hyperarousal, etc.

The existing bidirectional relationship between CI and psychiatric and/or somatic diseases is highly dependent on insomnia phenotype based on total sleep duration (see Classification). There is a growing body of evidence demonstrating that ISSD is associated with higher health risks and is the biologically more severe phenotype.^[11]

ISSD has been associated with an increased risk of grade 1 and 2 AH, accelerated atherosclerosis and ischemic heart disease, and chronic proinflammatory state, with ISSD being identified as a candidate risk factor for AH, alongside obstructive sleep apnea.^[50,51] The main mechanism behind deteriorated cardiovascular health in these patients is probably the increased activity of the HPA axis and increased sympathetic nervous system tone.^[52,53] Of particular note, ISSD is linked to increased risk of cardiovascular disturbances, unlike INSD or objective short sleep duration, without CI disorder.^[54]

Insufficient sleep has been also associated with broader hormonal imbalances, affecting appetite regulation and glucose metabolism, thus increasing the risk of metabolic disorders, particularly obesity and diabetes mellitus in ISSD.^[55] Sleep duration plays a crucial role, as demonstrated by the significantly increased risk of developing insulin resistance and type 2 diabetes in ISSD compared to INSD and non-insomniacs, mainly due to elevated basal cortisol levels and other counter-regulatory hormones.^[54,56]

The association of insomnia and psychiatric disorders such as recurrent depressive disorder is also much stronger with the ISSD phenotype. Furthermore, these patients are more frequently resistant to antidepressive therapy, which holds true in both adult and adolescents.^[8,57] On the other hand, INSD shows a tendency towards anxious-ruminative symptoms and the so-called “sleep misperception”.^[58]

Additionally, a notable difference is observed in the response to therapy between the two phenotypes of insomnia. INSD responds significantly better to cognitive-behavioral therapy for insomnia (CBT-I), while in ISSD, medication treatment leads to more effective and stable remission over time due to the suppression of physiological hyperarousal.^[59]Fig. 3 presents a comparative characterization of the two phenotypes in terms of distinctive features.

The bidirectional relationship between chronic insomnia and mental and somatic diseases underscores the complexity of the condition. Chronic insomnia can cause and aggravate mental health issues, cardiovascular problems, metabolic disorders, and cognitive impairments, while these conditions can, in turn, lead to or exacerbate CI. Additionally, insomnia can obscure the clinical presentation of almost any primary sleep disorder, which creates challenges in choosing the optimal treatment modalities and may increase overall health risk for the individual. This interdependence highlights the necessity for comprehensive treatment that considers both sleep and general health. Clinicians should prioritize the assessment of sleep quality in patients with chronic conditions and incorporate sleep interventions into their overall management to improve outcomes. This integrated approach can lead to more effective treatment strategies and improve the quality of life for individuals experiencing chronic insomnia and its associated complications

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The authors have declared that no competing interests exist.