Chronotype and Mental Health: Are Late Sleepers More Vulnerable?

Abstract

This review examines emerging evidence on the relationship between behavioral sleep timing and psychiatric disorders, highlighting the critical distinction between circadian preference (chronotype) and actual timing of sleep. These two concepts are not identical and show independent and interdependent impacts on a variety of mental health outcomes. Evidence suggests that actual sleep timing, rather than chronotype preference, is a stronger predictor of mental health outcomes, with late-night sleep patterns more consistently linked to poorer mental health across both cross-sectional and longitudinal studies. The mechanisms linking late night sleep patterns to poorer mental health are not well understood and cannot be fully explained by reduced sleep duration or being awake during the biological nighttime. Modifiable social and environmental factors likely play a role. Future research should clarify causal mechanisms and inform culturally sensitive, chronobiologically-informed interventions.

Introduction– Why Timing Matters

The etiology and expression of psychiatric disorders, including depression, anxiety, bipolar disorder, and schizophrenia, are increasingly being understood in new ways. While their specific neurobiological and genetic underpinnings remain central, growing attention is being paid to the moderating role of behavioral and physiological rhythms [1–3]. Among these, “chronotype” has emerged as a critical yet underappreciated dimension of mental health research [4]. Mounting evidence suggests that individuals with an evening chronotype (i.e., those who prefer sleeping later at night) are at heightened risk for a range of psychiatric conditions [1–3, 5–7]. While often congruent, behavioral timing—when an individual actually goes to sleep or wakes up, irrespective of preferred sleep timing—is becoming increasingly understood as an independent, clinically relevant risk factor for psychiatric disorders [8]. This distinction matters: chronotype is not necessarily aligned with or identical to sleep timing, as the latter may be influenced by life circumstances (e.g., work, family, friends), and these two factors may independently and interdependently impact mental health.

This review aims to synthesize emerging findings on chronotype and behavioral timing in the context of psychiatric disorders, with a particular focus on studies published within the past 1–3 years, underexplored mechanisms, and the role of cultural and genetic moderators. By doing so, we will underscore the crucial importance of accounting for individual differences in circadian preference and sleep behavior in both the prevention and treatment of psychiatric conditions.

Definitions and Conceptual Clarifications

The term “chronotype” has been used inconsistently across scientific literature, leading to some conceptual ambiguity. Originally, it referred to an individual’s preferred timing of sleep and activity within a 24-hour period [4]. Individuals were parsed into definite or moderate evening types, definite or moderate morning types, and an intermediate ‘neither’ category. This preference for sleeping during a specific part of the night is thought to be related to the function of the central circadian clock in the suprachiasmatic nucleus of the hypothalamus [9] perhaps as an expression of the phase angle of entrainment (the temporal relationship between an internal circadian marker (e.g., dim light melatonin onset) and a second marker associated with external time (e.g., bedtime)), which results from a combination of intrinsic circadian period length and the sensitivity to light [10, 11]. While the original definition of chronotype relied on self-assessment of the preferred time of day of activities, it has more recently been interpreted as the actual timing of behavior, especially on free days [8]. This latter conceptualization is likely a combination of intrinsic circadian function and societal and behavioral pressures.

The two most widely used tools for assessing chronotype are the Morningness-Eveningness Questionnaire (MEQ) [4] (or the reduced form of the MEQ [12]) and the Munich Chronotype Questionnaire (MCTQ) [8]. The MEQ captures subjective preference for activity timing, while the MCTQ relies on real-world sleep behavior—specifically sleep timing on work-free days—to estimate mid-sleep time as a measure of chronotype. In contrast to preference-based assessments, behavioral timing can also be measured objectively using tools like actigraphy, which imputes sleep–wake patterns through movement data.

The distinction between preferred and actual timing of behavior is especially relevant in modern societies, where social and occupational demands often override or mask innate biological rhythms. For example, an individual who naturally prefers waking later in the morning may be required to rise earlier for work and family obligations (even on work-free days), resulting in a habitual sleep schedule that misrepresents their underlying chronotype. Cultural norms, caregiving responsibilities, and work requirements can all force people into sleep-wake schedules that are misaligned with their natural timing preferences.

Genetic Heritability

Chronotype preference is often viewed as a biologically driven trait, but its genetic contribution to individual differences is relatively moderate. Twin and family studies conducted in the United States [13], United Kingdom [14], the Netherlands [15] and Brazil [16] estimate the heritability of chronotype preference (as assessed by the MEQ) at around 50%. In contrast, studies in more socially homogeneous populations, such as the Hutterites [17], report lower estimates of 14–30%. These findings suggest that while genetics contribute meaningfully to circadian preference, they do not fully explain its variability. The genetic underpinning of behavioral timing has not been well studied.

Across the lifespan, significant shifts occur in both chronotype and sleep timing. Adolescents typically experience a delay in their sleep timing and chronotype, while older adults gradually shift earlier [18, 19]. Sleep timing tends to stabilize in mid-adulthood, with approximately 60% of adults showing no significant clock timing shifts during this period [20]. An individual’s perception of how early or late they prefer to stay awake, especially those with intermediate chronotypes, can also change with work or school schedules, cultural norms, and lifestyle behaviors. Actual sleep timing is greatly influenced by these factors as well as light exposure patterns; these may account for a larger proportion of variability than common genetic variants [21]. As such, the relative association between the clock timing of sleep and chronotype can vary significantly by age and culture. For example, while an adolescent in Spain who goes to sleep at 11 pm might consider herself an early chronotype, an older American going to sleep at 11 pm might consider himself a late chronotype. These non-biological aspects of chronotype and behavioral timing increase the complexity of understanding the genetic contribution.

A small subset of people experience chronotypes defined by both their preference and actual sleep-wake timing, extreme enough to be considered pathological (i.e., advanced or delayed sleep-wake phase disorder [22, 23]). While there is no apparent pathophysiological consequence of having a significantly delayed (e.g., 4 am– noon) or advanced (e.g., 7 pm– 3 am) sleep schedule, these are far enough outside of societal norms that they can cause significant problems in maintaining social relationships and regular work [24, 25]. Several circadian clock-associated genes have been identified that underlie these extreme chronotypes [26, 27]. Targeted chronobiological interventions such as light therapy, melatonin supplementation, or structured circadian phase-shifting protocols may be used to help adjust these individuals to more moderate schedules, though these are not always successful [23, 28].

Recent Findings

Association of Psychiatric Disorders with Chronotype Preference

Chronotype preference has emerged as a significant vulnerability factor in mental health. While not a clinical diagnosis itself, eveningness is consistently associated with a higher prevalence and greater severity of psychiatric symptoms, including mood disturbances, anxiety, attentional difficulties, and emotional dysregulation [1–3, 5−7, 29].

In our recent analysis of more than 70,000 middle-aged and older adults in the United Kingdom (UK Biobank cohort), we found that self-reported evening chronotype preference was associated with a significantly higher prevalence of major depressive disorder, generalized anxiety disorder, and other psychiatric conditions [3]. Notably, these associations extended beyond cross-sectional patterns: survival analysis showed that evening types had a higher risk of developing these disorders over time, underscoring eveningness as a potential risk factor for future psychopathology [3]. These findings are supported by other studies demonstrating a consistent relationship between eveningness and elevated depressive symptoms [20]. This vulnerability is not limited to adults– a systematic review in youths found that eveningness was significantly associated with general mental health problems, mood-related disturbances, anxiety, increased risk for psychotic symptoms, and maladaptive eating behaviors [30]. Eveningness in students has also been linked to more frequent and severe feelings of defeat and entrapment, as well as suicidal ideation [31].

Association of Psychiatric Disorders with the Timing of Behavior

While chronotype preference provides valuable insights into mental health risk, emerging evidence suggests that the actual timing of behavior—when individuals habitually go to sleep and wake up—may be an even stronger predictor of psychiatric outcomes. Behavioral timing reflects the lived expression of sleep–wake rhythms and captures the combined influence of biological, social, and environmental factors.

In our analyses of the UK Biobank, we also examined objectively (actigraphy) measured sleep–wake timing to assess their independent associations with psychiatric outcomes [3]. We found that, as with chronotype, later behavioral timing was consistently linked to a higher prevalence of conditions such as depression, anxiety, and broader categories of mental and behavioral disorders. Crucially, this association persisted even after adjusting for chronotype preference, suggesting that actual sleep–wake patterns may exert a direct influence on psychiatric risk, independent of chronotype [3]. While later sleep timing is often associated with shorter sleep, individuals with later sleep timing had an increased risk for psychiatric disorders regardless of how much sleep they obtained, indicating that sleep quantity is not the sole driver of this association [32, 33].

Additional recent studies support these findings. In a community-based sample of older adult women, later sleep timing was associated with both depressive symptoms and an increased likelihood of surpassing the clinical threshold for depression, independent of sleep duration [34]. Similarly, a systematic review of pediatric populations found that later sleep timing in children and adolescents was linked to poorer emotional regulation, lower academic performance, and reduced cognitive functioning [35]. Evidence from forensic psychiatric populations further underscores this pattern [36]. Individuals in these settings are more likely to exhibit later behavioral timing than the general population, with the strongest evening preferences observed among those diagnosed with personality disorders [36].

A central theory of circadian research is that misalignment—a mismatch between an individual’s preferred sleep-wake timing and their actual behavioral schedule—is detrimental to mental health [37]. Misalignment has been linked to mood disturbances, metabolic dysfunction, impaired cognition, and increased psychiatric vulnerability [37–39]. Circadian misalignment can result from rigid schedules that force individuals to operate out of synchrony with their natural preferences, often leading to chronic sleep restriction, daytime fatigue, and elevated stress. Theoretically, aligning behavior with preference should mitigate these outcomes.

However, our findings—and those of others—suggest that synchrony between chronotype preference and behavior may not be the most decisive factor in determining mental health outcomes. While circadian misalignment is linked to poorer mental health outcomes, the timing of behavior itself appears to be a stronger and more consistent predictor of psychiatric risk [3]. While individuals with an evening preference who maintain a sleep schedule aligned with their internal clock still show elevated rates of depression, anxiety, and related disorders if their sleep–wake timing is late, evening individuals who maintain earlier sleep timing have lower rates [3].

This distinction highlights a key insight: it is not just the mismatch that matters, but the timing itself. While alignment between preference and behavior may offer some buffering effects, it does not eliminate the risks linked to late sleep-wake timing. Therefore, interventions to reduce psychiatric vulnerability should not only aim to reduce misalignment but also consider shifting behavioral timing earlier when feasible, regardless of chronotype.

These findings highlight an important, yet still unresolved, question: why is being awake late so detrimental to mental health? Unpacking the biological, environmental, and psychosocial mechanisms at play will be crucial for developing more targeted and personalized approaches to prevention and treatment.

What about Staying Up Late is Bad for You?

While the association between later sleep timing and worse psychiatric outcomes is well-documented, the underlying mechanisms remain poorly understood. Several non-exclusive factors may contribute to the increased vulnerability associated with being awake late at night, though these are all hypothetical at this point. Among the most likely factors involved in the association between being awake late at night and poor mental health outcomes are circadian misalignment, sleep loss, behavior, and light exposure (Fig. 1).

Fig. 1.

Conceptual model linking timing of behavior to psychiatric risk through multiple independent pathways. Chronotype and cultural/socioeconomic context (purple) shape the timing of behavior (orange), defined as the habitual timing of the sleep–wake schedule. Timing of behavior, in turn, influences downstream moderating mechanisms, including nocturnal vulnerability through reduced prefrontal cortex inhibition, altered brain connectivity, and compromised self-regulation (“the mind after midnight”, yellow), and neuroinflammation (blue). It may also contribute to mental health risk through social isolation and behavioral risk factors (grey), although empirical data directly linking these pathways to behavioral timing are currently limited. These pathways independently contribute to mental health and psychiatric risk (green). Arrows indicate proposed directional relationships based on current evidence. The model emphasizes the importance of both upstream contextual factors and downstream biological and psychosocial mechanisms in shaping psychiatric vulnerability

(1) Circadian misalignment. When some individuals stay awake late into the night, they are awake during a time at which the circadian clock is expecting sleep, the “biological night.” Staying awake during the biological night creates a mismatch between internal physiology and external demands that can have negative consequences on mood [40]. However, not everyone who goes to bed late is necessarily awake during their biological night; individuals with a delayed circadian phase may remain aligned with their internal clock despite a late schedule [22, 23].

(2) Sleep loss. Sleep loss disrupts neural communication and impairs emotional and cognitive regulation [41]. When periods of extended wake are coupled with circadian misalignment, it may create a uniquely vulnerable state, conceptualized as the “Mind After Midnight,” characterized by reduced cortical activity, altered connectivity, and compromised self-regulation [42]. During this state, emotional reactivity is heightened, and attention becomes biased toward negative or ambiguous information. This may be due to increased amygdala activity in the absence of the regulatory influence typically exerted by prefrontal regions during the day [42]. Simultaneously, changes in the brain’s reward circuitry may emerge. Neurochemical shifts, particularly involving dopamine, alter the sensitivity and balance of reward processing systems. Increased activity in regions like the ventral striatum (nucleus accumbens region) is paired with reduced engagement of the dorsal striatum (caudate and putamen), leading to a state in which the anticipation of reward is amplified, even as actual satisfaction is diminished. This neural profile may explain why late-night wakefulness is linked to increased impulsivity, risk-taking, and vulnerability to maladaptive behaviors [42].

(3) Behavior. Being awake late at night often occurs in social isolation, with limited access to supportive interactions, a key protective factor against mental health challenges. While individuals with an evening chronotype report significantly higher levels of loneliness and lower perceived social support, both established risk factors for depression and anxiety, comparable data are lacking for actual sleep–wake timing [44]. Thus, the psychosocial consequences of late behavioral timing remain an important but underexplored area of research. While individuals who rise early in the morning, and who have a lower burden of mental health disorders, also have a similar social isolation, there may be unique factors associated with late night social isolation, including different levels of homeostatic sleep pressure, the burden of a day’s worth of stress and anxiety, and difference in natural illuminance. Whether these factors contribute to the interaction of late-night behavior and social isolation is unknown.

(4) Light. Association studies have linked artificial indoor light exposure and adverse mental health outcomes in several large epidemiological studies [45, 46]. These studies, however, provide limited mechanistic evidence that the illuminance of nocturnal light to which individuals are exposed and have differential mental health outcomes are physiologically relevant [47]. For example, one recent study claimed that different mental health outcomes were associated with wrist actigraph-recorded illuminances of 0.5 lx, 0.8 lx, and 3.0 lx [46], all of which are far below the published sensitivity thresholds of hypothalamus-mediated light responses [48, 49]. The association between nocturnal light and mental health is more likely mediated by the behavior that light enables rather than a direct physiologic effect. Even dim indoor artificial light may allow for engagement in stimulating or emotionally charged activities, such as scrolling through social media [50], or engaging in less mental-health-promoting activities like drinking alcohol [51]. These behaviors can extend wakefulness and disrupt emotional regulation [50, 51].

Many epidemiological studies have also associated outdoor artificial light at night (ALAN) with negative mental health outcomes [52–54]. From a human physiology perspective, ALAN levels in residential areas are typically low, and the use of curtains, blinds, or other forms of indoor light shielding further reduces actual exposure to ALAN. As a result, most individuals encounter only minimal levels of outdoor light at night, making the direct physiological impact on mental health likely negligible. In addition, ALAN is highly confounded by urbanization: areas with higher outdoor light levels also tend to exhibit other features, such as noise pollution, higher population density, reduced green space, socioeconomic inequality, and increased nighttime activity, all of which can independently contribute to poor mental health outcomes [55, 56].

(5) Other considerations. It is essential to consider both economic and social factors in relation to the relationship between behavioral timing and mental health. Early bedtimes are associated with contextual and socioeconomic factors that may impact health. For instance, adolescents with earlier bedtimes often come from lower-resource environments and have reduced access to digital devices, the internet, and extracurricular activities [57]. Conversely, later bedtimes in youth are often associated with greater access to screens [58] and more autonomy over evening routines [59]. In adults, shift work [60], crowded living conditions, or caregiving responsibilities [61, 62] may also delay sleep timing, particularly in socioeconomically disadvantaged populations. These contextual influences can confound the relationship between sleep timing and mental health and may partially explain why late timing is more prevalent in certain demographic groups. Therefore, interpretations of behavioral timing must be situated within a social determinants of health framework, especially when assessing psychiatric risk in youth, underserved communities, or marginalized populations. Future research should actively examine how structural inequities, such as housing instability and occupational demands, intersect with sleep behaviors to shape health outcomes.

Controversies and Opportunities in the Research Landscape

There are ample opportunities to examine the relative contributions of the factors involved in sleep timing as well as physiological mechanisms that partially co-vary with sleep timing. These include accounting for sleep duration [32, 33], sleep regularity [63, 64], socioeconomic causes [65] and behavior during the extended nocturnal hours [66]. A further critical gap concerns the issue of directionality. It remains unclear whether late sleep timing contributes to psychiatric symptoms or results from them. For instance, individuals with depression may adopt later sleep schedules due to low motivation, hypersomnia, or disrupted routines, suggesting that altered timing is a consequence of mood disturbances. On the other hand, prospective studies suggest that late timing may precede and increase vulnerability to psychiatric symptoms through pathways such as circadian misalignment, emotional dysregulation, or reduced exposure to protective daytime activities. Longitudinal and experimental studies are urgently needed to disentangle these possibilities and establish causal relationships. Without clarity on directionality, intervention strategies risk being mistimed or ineffective.

Ultimately, understanding why and how the timing of behavior influences psychiatric health will be essential for developing personalized, chronobiologically informed approaches to prevention and treatment.

Conclusions and Future Directions

This review highlights the growing body of evidence linking sleep–wake timing—both in terms of chronotype preference and actual behavior—to psychiatric risk. While eveningness has consistently been associated with increased vulnerability to mood, anxiety, and behavioral disorders, emerging findings suggest that the timing of behavior itself—when individuals habitually go to sleep and wake up—may be an even stronger and more consistent predictor of mental as well as physical health outcomes [3, 41, 67]. This association persists even after accounting for chronotype preference and sleep duration, indicating a unique contribution of behavioral timing.

A key takeaway is the importance of distinguishing between preference and behavior. Chronotype preference reflects a biologically influenced tendency, whereas actual sleep–wake behavior captures the lived expression of that tendency as shaped by social, environmental, and cultural factors. Conflating the two may obscure important insights into psychiatric risk and resilience. Real-world behavioral timing appears to have greater predictive value for both mental and physical health outcomes and should be prioritized in future research and clinical assessments [3, 41, 67]. As such, prioritizing behavioral measures in research and clinical assessments is essential—a recommendation now formally endorsed by the most recent World Sleep Society guidelines [68].

Another key insight from this emerging literature is that while the link between late sleep timing and mental health problems is well-documented, the mechanisms underlying this association remain unclear. While wakefulness during the biological night and sleep deprivation may contribute to the adverse outcomes associated with late sleep timing, they are insufficient to account for all observed risks. The role of social isolation, cumulative stress during the daytime, natural light exposure, socioeconomic status, and other contextual factors all are likely to play an important role in explaining why there is an enhanced vulnerability to mental health disorders in individuals who have later bedtimes [46, 47]. There is a pressing need for culturally sensitive, personalized approaches to understanding and addressing circadian-related vulnerabilities. Sleep–wake timing and chronotype perception are context-dependent and can vary widely across age groups, cultural norms, and societal structures. What constitutes “early” or “late” behavior, just like “good” or “poor” sleep, is not universal, and interventions must account for these differences to be effective [69].

Ultimately, these insights have significant implications for psychiatric prevention and intervention strategies. Chronobiological interventions—such as light therapy and structured behavioral schedules—may be particularly beneficial for individuals with persistent late timing or irregular sleep patterns [70]. However, without a clear understanding of causal pathways and modifiable targets, such efforts risk being poorly timed or misdirected. Longitudinal and experimental studies are crucial for unraveling the directionality of effects and identifying critical windows for intervention.

Future research should continue to explore the interplay between preference, behavior, regularity, and environmental context to inform more nuanced and individualized approaches to mental health care. Integrating circadian science into psychiatric practice holds promise for enhancing prevention, early detection, and treatment outcomes.

Author Contributions

R.L. wrote the initial draft of the manuscript. J.M.Z. edited the manuscript. All authors reviewed the final manuscript.

Funding

This research was supported by the National Institute on Aging (NIA) through the NIH Pathway to Independence Award (K99/R00) under grant number K99AG08484.

Data Availability

No datasets were generated or analysed during the current study.

Declarations

Competing Interests

The authors declare no competing interests.