Insomnia as a transdiagnostic factor across chronic illnesses common to primary care: a narrative review

Introduction

Insomnia is a widely prevalent condition known to be highly comorbid with chronic medical and mental health conditions (1-4). Estimates of insomnia prevalence range from 10% to 50% with higher prevalence rates among minority ethnic groups, older adults, females, low socioeconomic status, and among those with chronic illness (5-10). Insomnia causes several detrimental effects on an individual’s health including deficits in cognitive, social, and occupational functioning, increased risk and worse prognosis for mental health and physical health conditions, and poor quality of life (4,11). Treatments for insomnia not only result in alleviation of insomnia symptoms and improvements in sleep quality but may also extend to improvements in clinical symptoms for comorbid conditions including mental health conditions (depression, anxiety) as well as physical health conditions like cardiovascular disease (CVD), type 2 diabetes, obesity, and chronic pain (12-15).

Insomnia consists of four primary symptoms: difficulty initiating sleep, difficulty maintaining sleep, nonrestorative sleep, early morning awakenings, and resulting daytime impairments due to these sleep disturbances (16). Further, studies have collectively proposed the possibility of two insomnia phenotypes, insomnia with short sleep duration and without short sleep duration. This distinction is important as research supports the notion that these two insomnia phenotypes may have different impacts. Insomnia with short sleep duration may be a risk factor for medical conditions, whereas both insomnia phenotypes may be a risk factor for psychiatric conditions, but via different pathways: psychological and behavioral, which are discussed in detail below (16-19).

Insomnia has been proposed as a transdiagnostic factor which contributes to the onset, maintenance, and exacerbation of psychiatric symptoms (16,20,21). Within a transdiagnostic framework, effective treatments can be developed to target shared mechanisms to reduce symptoms, severity and risk across complex comorbid conditions. We propose that certain transdiagnostic processes, namely insomnia with and without short sleep duration, may also extend to chronic medical conditions.

There are three lines of research that support insomnia as a transdiagnostic factor across chronic illness. First, insomnia is highly comorbid with mental health disorders (depression, anxiety, trauma, behavioral problems) as well as with chronic medical conditions (3,22). Second, insomnia can no longer be considered as an epiphenomenon or secondary to the primary disorder (16). Insomnia is a known risk factor for the development of certain medical conditions (23-26). For instance, insomnia increases the risk for developing or dying from CVD by 45% (27-29). Insomnia also increases the risk for type 1 and type 2 diabetes. Impaired sleep dysregulates glucose metabolism, alters insulin and glucose levels, and decreases insulin sensitivity (15). While not a required symptom of insomnia but instead a common consequence of insomnia, short sleep duration appears to be a prominent factor in increasing the risk for obesity and increased weight gain (30,31) which may subsequently increase risk for other chronic illnesses. Sleep disturbance also worsens pain severity, and predicts 38% of the variance of pain severity, anxiety and depression (15,32). Insomnia and fatigue are the most frequently reported residual symptoms following the treatment of mental health problems comorbid with chronic medical conditions and in turn have been found to be predictors for relapse and recurrence of depression and anxiety (33,34). Thus, there is a need to treat insomnia as a primary disorder and to incorporate cognitive-behavioral sleep treatments within the context of treating comorbid medical disorders as opposed to expecting insomnia to subside following treatment of another diagnosis (16). Third, neurobiological and treatment research has identified causal mechanisms through which insomnia may influence medical symptomatology. While specific mechanisms are still being explored, insomnia with short sleep duration has been linked to cardiometabolic and neurocognitive morbidity via activation of both limbs of the stress system (17). Physiological markers of insomnia have also been identified using polysomnography (PSG), beta frequency waves in the electroencephalogram (EEG) which have linked insomnia to chronic illnesses such as hypertension, diabetes, pain, depression, and mortality (18). These have been described in detail when discussing the direct relationships between insomnia and chronic illness.

Reductions in insomnia symptoms have been linked to a reduction of symptoms of depression and anxiety, fatigue, visits to primary care, nicotine and caffeine use, and has improved treatment adherence and medical symptomatology such as pain severity, ratio of day and night cortisol, and frequency of headaches (13,35-39). Cognitive behavior therapy for insomnia (CBT-I) has been found to reduce CVD risk through an improvement in biomarkers such as high-density and low-density lipoprotein, triglycerides, hemoglobin A1c, glucose, insulin, C-reactive protein, and fibrinogen as well as improvements in daytime symptoms of heart failure, fatigue, physical functioning and, at 6-month follow-up, anxiety and depression (40). Thus, the impact of insomnia as a transdiagnostic factor cannot be overlooked.

Overall, comorbid mental and physical health disorders result in greater symptom severity, functional, social, and occupational impairment and therefore require longer treatments (21,41). A better understanding of the mechanisms through which insomnia impacts chronic medical and mental health conditions can help augment treatments for these comorbid conditions. The public health implications of efficacious, behaviorally-based, transdiagnostic treatments would be significant as these would be both time and cost-effective with few to no adverse effects. Thus, treatments would be easier to implement in medical settings, would make mental health care more accessible to patients, and would have the potential to concurrently treat comorbidity (16).

Objectives

The purpose of this review is to propose a novel empirically-based theoretical model presenting insomnia as a transdiagnostic factor across chronic medical illnesses commonly seen in primary care settings, to describe the shared psychological and behavioral mechanisms through which insomnia influences these chronic illnesses, and to propose psychological and behavioral clinical recommendations specific to primary care based on these findings. To limit the scope of this review, we will focus on four chronic medical conditions commonly seen in primary care: CVD, diabetes, obesity, and chronic pain. To our knowledge, this is the first study that delves into summarizing the current literature on the insomnia-chronic-illness relationship with a focus on the psychological and behavioral mechanisms. Given studies have identified insomnia with short sleep duration as particularly relevant in increasing risk for medical comorbidities (17,18,42) in addition to presenting research on insomnia with and without short sleep duration, articles on short sleep duration alone (but not specifically identified as insomnia) have been included. We present this article in accordance with the Narrative Review reporting checklist (available at https://amj.amegroups.com/article/view/10.21037/amj-24-21/rc).

Methods

The following databases were used to identify articles related to the relationships between insomnia, chronic illness, and psychological and behavioral mechanisms: Google Scholar, PsycINFO, Science Direct, and PubMed. See search summary table (Table 1) for additional details pertaining to keywords, inclusion and exclusion criteria and selection process. All titles, keywords, and abstracts were scanned to determine if they met inclusion criteria. Representative articles that pertained to the relationships between insomnia and chronic medical illness in adults 18 and above were included in this narrative review. The search flow for articles is presented in Figure 1.

Figure 1 Flow of the study search.

As few studies have explored the direct relationships between insomnia and chronic illness, the search for additional relevant articles was divided into three steps. First, to find articles that studied the direct effects of insomnia on chronic illnesses (pathway 1; see Figure 2). Second, to find articles that studied the effect of insomnia on a potential mechanistic factor (psychological and behavioral; pathway 2). And third, to find articles that studied the effect of the mechanistic factor on the chronic illness (pathway 3).

Figure 2 Pathways representing the impact of insomnia on chronic illness.

Following identification of articles, each article was categorized based on the specific pathway represented. Next, each article was reviewed based on several factors to succinctly summarize articles. These factors included the direction of the relationship of variables, study design, independent variables, dependent variables, covariates, demographic factors (sample size, type of population, percent female, age range and country), and summary of relevant findings.

Articles were then organized into tables based on these factors which delineated the psychological and behavioral pathways that could potentially mediate or moderate the relationship between insomnia and chronic illness. Table 2 includes a summary of articles that focus on the direct relationship between insomnia and the specific chronic illness (pathway 1). Table 3 includes representative studies examining the effects of insomnia on the specific mechanistic factor: psychological and behavioral (pathway 2; see Figure 2). Tables 4-7 represent articles that focus on the impact of a psychological or behavioral mechanism on the specific chronic illness (pathway 3). Table 4 represents articles pertaining only to CVD. Table 5 represents articles pertaining only to diabetes. Table 6 represents articles pertaining only to obesity. And Table 7 represents articles pertaining only to chronic pain. As the tables include detailed summaries of the articles, the description of these pathways in the text emphasizes the overall shared mechanisms that were identified and provide a summary of findings from each mechanistic pathway. Please see the tables for details on specific articles.

Results: shared mechanisms between insomnia and chronic medical illness

The direct impact of insomnia on chronic medical illness (Pathway 1, Table 2)

Several studies have differentiated between objective and subjective measures of sleep disturbance and consequentially propose two insomnia phenotypes indicated to differentially impact chronic illness: insomnia with short sleep duration and without short sleep duration (16,18,19). Objective measures of sleep include actigraphy or PSG which provide accurate measurements of quantity of sleep whereas subjective measures of sleep include a persons self reports of insufficient sleep, sleep quality, or dissatisfaction with sleep. A prominent factor that directly impacts chronic illness outcomes was insomnia with short sleep duration, particularly that below 6 hours per night (43,44). The National Sleep Foundation recommends sleep duration for adults is between seven to nine hours (166). Insomnia with short sleep duration is linked to cardiometabolic and neurocognitive morbidity via activation of both limbs of the stress system, i.e., the hypothalamic-pituitary-adrenal (HPA) axis, the sympatho-adrenal medullary axis (SAM), and activation of the inflammation system (17). Meta-analyses have found increased risk of between 11% and 27% for acute myocardial infarction, coronary heart disease, heart failure, stroke or a combined event in individuals with sleep-onset and sleep maintenance problems (29); while another systematic review found a 45% increased risk for morbidity and mortality from CVD in those with comorbid insomnia symptoms (27). The magnitude of risk appears to vary due to differences in measuring and reporting insomnia symptoms (26). Similarly, individuals sleeping less than 6 hours are at greater risk for diabetes whereas those sleeping more than 6 hours were not (49,167). In those with pre-diabetes, short sleep duration leads to insulin resistance and hinders glucose control after controlling for confounding variables like physical activity, energy intake, demographics, and other medical conditions (50). In those with obesity, physical activity increased with longer sleep durations; however, there did not appear to be a direct impact of short sleep duration on body mass index (BMI) (52). However, a meta-analysis and systematic review found that those with insomnia are about 1.3 times more likely to have metabolic syndrome related symptoms (hypertension, hyperlipidemia, hyperglycemia and obesity) (53). Finally, short sleep duration has also been found to impact chronic pain onset in both cross-sectional, randomized controlled trials, and longitudinal studies (57-61). It is important to note that there are some studies that did not find a significant association between short sleep duration and chronic illness (45,50,52). Thus, there is a need for more longitudinal studies to explore the relationships between short-sleep duration and chronic illness, as well as explore other factors that may play a role.

A second insomnia related variable that impacts chronic illness management is sleep quality. Sleep quality is defined as whether a person is satisfied with their sleep overall and whether they feel refreshed upon waking (19). Notably, sleep quality is a separate construct from fatigue, daytime sleepiness, and depression (19). Sleep quality is a person’s satisfaction with sleep initiation, maintenance, and quantity (168). A high percentage of individuals with chronic illness have poor sleep quality, for example: 43% of those with CVD and 59% of those with obesity (46,54). Insomnia also affects health related quality of life (HRQOL), and there is a need to better understand how poor sleep affects self care behaviors in those who are managing a chronic illness (51).

Although a majority of the studies reviewed supported a relationship between objective sleep duration and subjective sleep quality with chronic illness, a few studies did not (45,109). Some studies with non-significant findings had a smaller sample size and limited generalizability (college student sample vs. clinical samples), but one longitudinal study with a larger sample size also found non-significant relationships between insomnia and CVD (45). A majority of studies were cross-sectional and so there is a need for more longitudinal and intervention based studies.

Finally, several physiological mechanisms have been reviewed that highlight the relationship between insomnia and chronic illness but are not described in detail here to limit the scope of this review on psychological and behavioral mechanisms (17-19). Briefly, studies have identified physiological markers of insomnia including sleep variables identified using PSG, beta frequency waves in the EEG, cortisol levels, heart rate/sympathetic activation, multiple sleep latency test (MSLT), blood pressure, blood glucose, metabolic rate, inflammatory markers, immune system deficits, ghrelin/leptin assays, and levels of gamma-aminobutyric acid (GABA) in the brain (18) which have linked insomnia to chronic illnesses such as hypertension, diabetes, pain, depression, and mortality (18). Findings from these reviews indicate two insomnia phenotypes and differential impacts on physical and mental health. The first insomnia phenotype (with short sleep duration) may be a risk factor for medical conditions, whereas both insomnia phenotypes (insomnia with short sleep duration and insomnia with normal sleep duration) may be risk factors for psychiatric conditions but via different pathways (17). However, it is important to recognize that although the second insomnia phenotype may not have a direct impact on chronic illness, it has the potential to indirectly affect chronic illness and chronic illness management via factors such as worry, rumination, sleep misperception, and mental health concerns like depression and anxiety, which influence health behaviors (diet, physical activity) and treatment adherence. There were a greater number of studies exploring mediating and moderating factors that may influence this relationship. Below, we will present these factors as either psychological or behavioral mechanisms and will summarize how they might impact the relationship between insomnia and chronic illness.

Psychological mechanisms (Pathways 2 and 3)

Cognitive factors

Worry and rumination

Worry and rumination are both classified as types of perseverative cognition (169-171) with worry linked closely to anxiety; whereas rumination is linked to depression (62,170). Several studies, including Harvey’s cognitive model of insomnia, suggested that individuals who suffer from insomnia tend to be overly worried about their sleep and about the daytime consequences of not getting enough sleep (i.e., sleep specific worry) (16,151). Studies find that poor sleepers tend to report greater daytime rumination (unrelated to sleep) compared to good sleepers (62-64). A poor nights sleep also leads to worse mood during the day including irritability, anxiety, nervousness, anger, sadness, or other mood fluctuations and can also amplify negative moods or temperaments (16,80). For instance, if a person has a temperamental trait of neuroticism then their tendency to worry, ruminate, or experience other negative emotions may be amplified with poor sleep.

Within the context of chronic illness management, worry or rumination appear to be common concerns and may relate to adjustment and coping with illness, medication management, treatment adherence and so forth. Worry and rumination also predicts medical outcomes. For instance, worry influences heart rate variability (102), blood pressure, and medication adherence in those with coronary heart disease (103). In those with diabetes, diabetes distress, which refers to worries and concerns about how having diabetes will affect them, and distress surrounding how management of medications may work was a common concern (119). Additionally, different kinds of rumination (angry rumination had a greater impact than sad rumination) were found to affect heart rate, diastolic and systolic blood pressure. Rumination due to depression and hostility appeared to lead to repetitive cardiovascular activation with implications for cardiovascular health (104). Similarly, worry and rumination (or perseverative thinking like pain catastrophizing) also has the potential to lead to weight gain and worsen chronic pain and pain severity (58,132-134,151-153,156,172). Most of the evidence surrounding how insomnia, worry, and rumination affect medical concerns has been limited to cardiovascular illnesses. There is also a need to better understand how these factors affect health behaviors like treatment adherence, physical activity, smoking, alcohol use, and eating behaviors (47). The added impact of mental health difficulties adds complexity to prognosis and treatment protocols within the context of chronic illness management (173,174). Recent studies have focused more on the impact of worry and rumination on development of insomnia and so more longitudinal studies are required to better understand the directionality of these relationships (175,176). It is interesting to note that given the overlap between the constructs of worry and anxiety, and rumination and depression, worry and rumination were found to have specific effects in the insomnia-chronic illness relationship. Future research should also focus on disentangling the differential impacts of worry and rumination and how depression and anxiety may have unique components beyond worry and rumination that may influence this relationship.

Depression and anxiety

Research has strongly supported the high prevalence of insomnia or sleep disturbances in those with depression and anxiety disorders (22,33,71). One study found that insomnia increased the risk for depression by 18 times in a large sample (72) (see Table 3). Insomnia with and without short sleep duration have been associated with anxiety and depressive symptoms in comorbid psychiatric conditions (73,74). The mechanisms through which insomnia, depression and anxiety are related are complex and bidirectional (177,178). Depressive thoughts, rumination, and worry may cause difficulties in initiating and maintaining sleep at night. And during the day, the lack of sleep may induce more depressive and anxiety symptoms. Both daytime (fatigue, sleepiness) and nighttime symptoms (poor sleep quality, long sleep latency, time awake at night) of insomnia were significantly associated with depression and anxiety (post-traumatic stress disorder, social anxiety, panic attacks, generalized anxiety disorder) with daytime symptoms having a stronger association (81). Additionally, daytime symptoms were more strongly related to depression than anxiety (81). Finally, poor sleep worsens the effects of cognitive arousal and intrusions on the development of a depressogenic mindset (75). While two longitudinal studies have found strong associations for the link between insomnia and depression (76,179) more are required.

Depression and anxiety are also both common mental health problems in those with chronic illness and affect treatment adherence and other health behaviors like diet and physical activity which are important components of chronic illness management (105-108,120,121,139,157,158). Insomnia also appears to worsen premorbid depression in those with chronic illnesses (77,159). The mechanisms through which depression and anxiety affect chronic illnesses has been extensively researched. Briefly, these mechanisms include physiological pathways (such as the HPA axis, inflammation), adverse health behaviors (such as smoking, inactivity, adherence), HRQOL, and traditional risk factors (such as low density cholesterol, low heart rate variability, coagulation, hypertension) (78,105,122,140,180) (Tables 3-6).

Cognitive functions (attention, concentration, memory, problem solving)

Insomnia affects cognitive and executive functioning especially memory, concentration, attention, and problem solving (see Table 3). Common complaints observed by those with insomnia include attention deficits, memory loss, working memory, dual-tasking, reaction time, difficulty concentrating and difficulty with problem solving during the day with effect sizes ranging from the small to moderate range (65-68,181). Both short sleep duration and sleep quality perception appear to affect cognitive and executive functions during the day (65,68,69). The evidence on how poor sleep affects cognitive and executive functioning is mixed and somewhat depends on the type of tasks. For example, it seems that poor sleep affects complex attentional tasks more than simple tasks. As cognitive demands increase the cognitive dysfunction becomes more evident (70). Although the effects of poor cognitive functioning on chronic illness management have not been extensively researched, it is understandable that these deficits on a day-to-day basis have the potential to negatively affect those with complex medical regimens such as for patients with diabetes, thus interfering with treatment adherence and health behaviors (diet and physical activity) in turn affecting physical health outcomes. For instance, poor memory can affect whether someone remembers to take their medication on time. Problem solving difficulties can result in difficulties with making decisions and can affect treatment adherence and motivation to stick to health behaviors (65).

Emotional factors

Emotion regulation

Emotion regulation is the set of processes through which an individual modifies the occurrence, intensity, and duration of emotional experiences, expressions, and physiology in response to contextual demands and may be either adaptive or maladaptive (182-184). Insomnia and poor sleep predict emotion dysregulation, reduced positive affect and increased negative affect, and these findings have been supported by both cross-sectional and longitudinal studies (see Table 2) (79-86,154). Studies also suggest that emotion regulation may be a mediator between insomnia and depression and anxiety (81,87).

Emotion regulation also predicts physiological outcomes (see Tables 3-6). For example, emotion regulation affects cardiometabolic health via heart rate variability, vagal tone, inflammatory cytokines, and high risk metabolomics which interact with high risk health behaviors (110). In those with diabetes, emotion regulation appears to influence diabetes distress and consequentially diabetes management and glycemic control (123-125). The relationship between emotion regulation and obesity has been researched extensively and findings suggest that emotion dysregulation leads to emotional eating or overeating and as a result weight gain (135-137). Interestingly, reduced trait emotional intelligence and emotion suppression have been linked to obesity severity (138). Finally, maladaptive emotion regulation strategies have also been related to chronic pain and tend to worsen pain, increase disability and lead to depression (155). There is still a need to understand how insomnia and chronic illnesses may be related to specific emotion regulation strategies. Individuals with insomnia typically use maladaptive emotion regulation strategies like suppression, worry, rumination compared to those who do not have insomnia (83).

Behavioral mechanisms (Pathways 2 and 3)

Behavioral mechanisms through which insomnia affects chronic illness primarily include treatment adherence and health behaviors (physical activity and diet/eating behaviors). Avoidance and escape behaviors such as experiential avoidance, avoidance of movement, fatigue related avoidance were considered for this review, however, there were not sufficient articles that studied the relationships between insomnia, avoidance behaviors, and chronic illness to include. Insomnia can directly affect behavioral factors which in turn influence chronic illness. Alternatively, insomnia can indirectly affect behavioral factors via some of the psychological factors mentioned above (worry, rumination, depression, anxiety, memory, emotion regulation) (48).

Treatment adherence

Treatment adherence in those with chronic illness is typically suboptimal, worsens following hospital discharge, and is often complicated and made worse by mental health concerns such as depression (111,142,160,185). Studies support two alternate ways through which sleep can affect treatment adherence. The first is that better sleep leads to an improved understanding of the treatment plan (complex medical regimens, cost, possible adverse effects), in turn improving treatment expectations, which has been linked to lower dropout rates (88,89,112). Second, insomnia is a strong indicator of poor quality of life, and people are likely to become increasingly frustrated due to lack of good sleep. As a result, people are more motivated to make a change as the impact of poor sleep is immediate and easily recognizable (89). Thus, interestingly, it has been found that greater insomnia severity leads to more mental health visits and better adherence to mental health treatment, depending on the type of chronic illness (90,91).

Research has focused mainly on the relationship between insomnia and treatment adherence within the context of mental health visits and sleep specific treatment. For instance, those with insomnia and dysfunctional beliefs about sleep have poorer continuous positive airway pressure (CPAP) adherence (91,92). Treatment adherence interventions have also led to improvements in cardiovascular, diabetes, obesity, and pain outcomes (113,126,127,143,144,161). Adhering to healthy behaviors among those with chronic illness has also been related to perceptions of personal control and an understanding of consequences of illness (115). More research is required to better understand how treatment of insomnia affects treatment adherence for chronic illnesses (such as medication management) and mental health concerns (like depression and anxiety) due to mixed findings (93,114).

Health behaviors

Physical activity

It has been well established that adults who sleep poorly are less active than their counterparts due to daytime sleepiness and fatigue (94). Longitudinal studies have found that poor sleep quality or insomnia symptoms predicted lower levels of physical activity 2 to 7 years later (116,145). Those with chronic illness are more likely to report low physical activity, greater TV watching, and poor sleep duration (128,146,147). Physical activity is often a health recommendation for those with (and without) chronic illness and can lead to improved health outcomes for those with CVD, diabetes, obesity and chronic pain (116,129,162). Adults with insomnia symptoms were found to have lower cardiovascular fitness than adults without insomnia, potentially due to daytime sleepiness and fatigue (94).

Sleep variables such as subjective sleep quality, subjective sleep latency, and actigraphy measured sleep efficiency predict physical activity the following day. Studies have found that an increase in time to fall asleep was associated with a decrease in next day exercise duration and a 10% increase in sleep efficiency was associated with a 5.4% increase in next day moderate to vigorous physical activity (55,94). Greater morning-ness (i.e., a circadian rhythm aligned with early morning waking) and an earlier habitual wake time were also associated with greater levels of physical activity (51). To our knowledge, no studies have explored the impact of insomnia treatments (e.g., cognitive behavioral therapy for insomnia) on subsequent physical activity, which would provide more clarity on causal relationships between insomnia and physical activity. Experimental studies exploring causal pathways between sleep restriction and physical activity in adults have found mixed results with some studies reporting no change in physical activity following short sleep (95,96), but appearing to reduce physical activity in adults at risk for type 2 diabetes (186). Finally, the relationship between sleep and physical activity appears to be bidirectional. More physical activity during the day also leads to improved sleep at night (163,187).

Diet and eating behaviors

Improved diet and eating behaviors are also a common health recommendation to manage chronic illnesses particularly CVD, diabetes, chronic pain, and obesity. Sleep deprivation was found to lead to more daytime eating and binge eating, which in turn is associated with with increased medical morbidity and risk for cardiovascular problems, obesity, and type 2 diabetes (50,97,130). Those with insomnia also tend to eat less healthy foods and high caloric foods (95,96,98,148). Sleep restriction was found to lead to unhealthy food choices and increased energy intake reciprocally (117). Sleep is related to metabolic and hormone (ghrelin and leptin) disruption which contribute to unhealthy eating, increased appetite for carbohydrate dense foods and higher intake of sweet foods and snacks (50). Prolonged wake after sleep onset and greater sleep fragmentation have been linked to higher dietary restraint (188). Mediators for sleep and eating include psychological factors like depression, anxiety, and emotion regulation (30,56,81,99,136,141). Insomnia is also associated with eating disorder pathology and would be an area for future research (100).

Diets (like the Mediterranean diet) consisting of higher intake of fruits and vegetables, fish, olive oils, and dairy were associated with lower risk for chronic illness (CVD, diabetes, obesity, and chronic pain) (50,117,118,131,164). In those with obesity, diet and night eating was an important factor frequently explored in the literature and was associated with depression, anxiety and sleep disturbance although the directionality of these relationships have not been explored (148-150). Fewer studies have explored the impact of nutrition and diet on chronic pain although this relationship has been explored within the context of broader lifestyle factors (165).

Discussion

The aim of this review was to evaluate whether insomnia is a transdiagnostic factor across chronic medical conditions and to describe the shared psychological and behavioral mechanisms through which insomnia influences chronic medical illnesses that are commonly seen in primary care settings, and integrate and summarize research, and gaps in this area.

Findings from the review suggest that insomnia and insomnia symptoms are cross-cutting transdiagnostic factors across chronic medical illnesses specifically including CVD, diabetes, chronic pain, and obesity. Insomnia affects the development and prognosis of chronic illness directly and indirectly via shared psychological, and behavioral mechanisms. Psychological mechanisms (cognitive and emotional mechanisms) identified in the literature include worry, rumination, cognitive functions, emotion regulation, depression, and anxiety. Although, some of these factors (e.g., worry, rumination) overlap with depression and anxiety, it is important to recognize that subclinical factors that influence the development of depression and anxiety also appear to play a mechanistic role. Behavioral mechanisms identified in the literature included treatment adherence and health behaviors including physical activity and diet.

The empirically based model proposes that insomnia influences biological components of chronic illness directly and indirectly via the identified psychological and behavioral factors (see Figure 3). We recognize that several of these factors mutually influence each other; however, as the focus of this study was to explore the influence of insomnia, we have emphasized the unidirectional effects of insomnia on these factors. We also recognize several physiological mechanisms that impact the insomnia-chronic illness relationship (18). Finally, the purpose of this model is to offer a framework for clinical conceptualization and future research within the context of an integrated health care setting.

Figure 3 An empirically based theoretical model representing psychological and behavioral factors through which insomnia acts as a transdiagnostic factor across chronic medical illness.

Clinical implications and recommendations

The overlap between insomnia, mental health difficulties, and medical conditions adds to the complexity of patients seen in primary care settings and emphasizes the need to integrate psychological interventions within medical settings to treat both sleep and mental health conditions through integrated healthcare models (189). Insomnia is frequently overlooked in primary care despite its impact on psychological and physical wellbeing (68,190,191).

Providers should consider how sleep could play an integral role in improving mental health and physical health outcomes by using a biopsychosocial conceptual framework. Mechanistic factors proposed in our theoretical model including psychological factors such as worry, rumination, depression, anxiety, cognitive functioning, emotion regulation and reciprocal impacts on behavioral factors like treatment adherence, physical activity, diet and eating behaviors should be taken into consideration when providing treatment to those with chronic illnesses. It may also be helpful to make distinctions between insomnia with and without short sleep duration and target these with appropriate treatment components for insomnia.

Insomnia is a relatively simple and effective treatment target that yields excellent clinical outcomes in a short span of time. The first line of treatment for insomnia is CBT-I which lasts, on average, six-sessions with long term improvements that are maintained at three, six and 12 month follow up, with about 70% to 80% of patients reporting modest to large improvements in sleep onset latency, awakenings following sleep onset, sleep quality, sleep duration, and satisfaction (14,78,192-196). This can be particularly valuable in a fast paced setting like primary care. An added advantage that psychological treatments have over pharmacological treatment is the lack of dependency and tolerance effects and risk of relapse which are common with sleep medication (194). Further, CBT-I has been demonstrated to be effective in primary care settings and can be delivered through either individual or group modalities (14,101). CBT-I groups within primary care settings may allow for access to wider and diverse range of patients who might not otherwise receive specialized treatment for insomnia due to limitations in accessing healthcare and the lack of trained clinicians in behavioral sleep medicine (197). This may further address significant sleep disparities among racial and ethnic minority populations (5-7,9). Using CBT-I earlier on in treatment can also help boost rapport with patients who might be skeptical about psychological interventions or who may experience mental health stigma. Sleep deprivation has been normalized in our society and it may be easier for some patients to discuss difficulties with sleep compared to other types of mental health issues. Treating sleep first can also allow providers to gain the patient’s confidence regarding the efficacy of psychological and behavioral interventions given the relatively immediate improvements that follow from behavioral sleep recommendations. Finally, CBT-I has also been found to be effective for patients with comorbid mental and physical health conditions and thus, does not contraindicate their use with these populations (48,198).

It is important to acknowledge the medical complexity of patients that present to primary care settings, particularly those with comorbid mental and physical health conditions. It is also recognized that most of these relationships between sleep, mental health and chronic illness are reciprocal. However, we reason that sleep is a highly modifiable and optimizable factor that if treated can yield improvements in a variety of areas which could later be capitalized on when dealing with more complex treatment targets.

It is recommended that the above evidence-based model should be used as a framework for clinical conceptualization, treatment planning, and future research to understand the impact that insomnia can have on chronic illness. Additionally, it is proposed that primary care settings should consider the following suggestions to treat sleep disturbance:

• Primary care settings should incorporate routine screeners and assessments for poor sleep in patients presenting with chronic medical conditions. Some brief and well-validated screeners for sleep include the Pittsburgh Sleep Quality Index, Epworth Sleepiness Scale, Cleveland Sleep Habits Questionnaire (199), and the Sleep Disorders Symptom Checklist-25 (200). The SDS-CL-25 is a comprehensive primary care friendly screening instrument for a variety of sleep disorders (200).
• Healthcare providers should receive training on how to screen and assess for sleep problems in primary care settings. Psychologists in primary care settings should receive training in CBT-I to treat sleep disturbances.
• Integrated health care teams should consider inclusion of psychologists to provide CBT-I to patients with insomnia in addition to targeting other mental health concerns.
• Potential psychological (e.g., anxiety, depression) and behavioral (e.g., treatment non-adherence) mechanisms of the insomnia-chronic illness relationship should be assessed for, treated, and considered within the context of possible sleep disturbances (e.g., symptoms of insomnia).

Future directions for research

There is a need for rigorous research on the impact of insomnia on chronic illnesses due to varying definitions of insomnia and subsequent heterogeneity of findings. Future studies should explore the complex interactions between insomnia, mental and behavioral health, and chronic illness within the context of development of these illnesses as well as impact on prognosis. Some factors that were explored based on an initial search but excluded from our model were positive and negative emotions and cognitive distortions (e.g., irrational beliefs including catastrophizing, all or nothing thinking, overgeneralization, magnification, and personalizing) due to lack of sufficient information to draw inferences based on the available research (110). It is important to note that as this study was not a systematic review, future research should attempt to conduct systematic reviews or meta-analyses on specific pathways (considering that the full model may be too broad for a systematic review or meta-analysis). Finally, while some studies have explored the efficacy of CBT-I in comorbid insomnia (201) additional studies should explore whether CBT-I leads to improvements in insomnia in those with both psychological and medical comorbid conditions, explore long-term mental health and physiological effects and outcomes, determine mechanistic factors, and whether improvements in insomnia lead to improvements in these comorbid conditions. There is a need for randomized controlled trials, efficacy trials, and longitudinal studies in addition to cross-sectional studies exploring the complexities of these relationships. It would also be helpful to explore differences between subjective and objective measures of sleep within the context of chronic illness. Finally, social, and cultural mechanisms can also be explored within this context.

Limitations

It is important to note that this study was not a systematic review of the literature. We have attempted to summarize the literature to best represent the current state of research exploring the relationship between insomnia, psychological and behavioral health, and chronic illness and propose a unified conceptual framework. However, this study was not a comprehensive review of all available articles. A second limitation of this study is that we did not include social and cultural factors that would affect this relationship as this was outside the scope of this paper.

Conclusions

This study aimed to explore insomnia as a transdiagnostic or cross-cutting factor across chronic illnesses including CVD, diabetes, obesity, and chronic pain and explore the psychological and behavioral mechanisms that can influence this relationship. Furthermore, we aimed to integrate and summarize the available literature reviewing these relationships. There was sufficient evidence supporting insomnia as a transdiagnostic factor across chronic medical conditions. Several psychological (worry, rumination, cognitive functions, depression, anxiety, emotion regulation) and behavioral (treatment adherence, physical activity, diet and eating behaviors) factors were identified that appear to influence the insomnia-chronic illness relationship. We strongly recommend the assessment and treatment of insomnia and related psychological and behavioral factors in primary care settings to increase access to behavioral sleep interventions as well as to augment current treatments for chronic illness. Future research should explore these factors longitudinally and conduct intervention-based studies to see if improvements in insomnia lead to clinical improvements in other comorbid conditions.

Acknowledgments

None.

Footnote

Reporting Checklist: The authors have completed the Narrative Review reporting checklist. Available at https://amj.amegroups.com/article/view/10.21037/amj-24-21/rc

Peer Review File: Available at https://amj.amegroups.com/article/view/10.21037/amj-24-21/prf

Funding: None.

Conflicts of Interest: Both authors have completed the ICMJE uniform disclosure form (available at https://amj.amegroups.com/article/view/10.21037/amj-24-21/coif). The authors have no conflicts of interest to declare.

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