Advertisement

  • Loading metrics

Open Access

Review

The mechanisms underlying the effects of heat on mental health: A narrative review

Abstract

While recent studies have advanced our understanding of how heat affects mental health, the underlying mechanisms of this relationship remain fragmented. Previous reviews have emphasized broad and general physiological, psychological, behavioural, and social pathways, often neglecting the heterogeneity of mental disorders in terms of vulnerability and outcomes. We conducted a narrative review to tackle this gap and propose an outcome-oriented framework to better integrate evidence on heat-related mental health risks. We searched PubMed and Google Scholar from January 2023 to September 2025 and conducted backward citation tracking of relevant reviews and primary studies, with no restrictions on publication language, date, or article type. The review focuses on two distinct yet interrelated pathophysiological-related outcomes: (1) exacerbation of pre-existing mental health disorders, and (2) heat-related illnesses such as heat exhaustion and heat stroke. Moreover, we integrated these pathways to six psychiatric conditions most established as heat sensitive: organic disorders (International Classification of Diseases-10th Edition F00-F09), substance misuse (F10-F19), schizophrenia (F20-F29), bipolar disorders (F31), neurotic disorders (F40-F49), and suicidal behaviour (X60-X84). First, our findings show that heat exposure can exacerbate symptoms in individuals with schizophrenia, bipolar disorder, anxiety disorders, and suicidal behaviour. Key mechanisms include (i) neurotransmitter imbalances, (ii) physiological stress, and (iii) sleep disruption. Second, heat exposure can contribute to heat-related illnesses, particularly among individuals with organic disorders, substance misuse, schizophrenia, and bipolar disorder due to (i) ineffective thermoregulatory behaviours, (ii) impaired neuropathways, and (iii) interactions with psychotropic medications or substances. By mapping outcome- and diagnosis-specific pathways, this review offers a more integrated understanding of how heat impacts mental health. This approach may help clinicians anticipate exacerbations and guide tailored interventions. It also provides a conceptual basis for future, precise, mechanism-driven research questions and for policymakers to design targeted adaptation strategies in public health.

Citation: Corvetto JF, Bahls S-C, Barteit S, dos Santos Ferreira JV, Müller TJ, Sauerborn R (2026) The mechanisms underlying the effects of heat on mental health: A narrative review. PLOS Clim 5(6): e0000958. https://doi.org/10.1371/journal.pclm.0000958

Editor: Cheng He, Harvard University, UNITED STATES OF AMERICA

Published: June 8, 2026

Copyright: © 2026 Corvetto et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Funding: The author(s) received no specific funding for this work.

Competing interests: The authors have declared that no competing interests exist.

Abbreviations: ADHD, attention deficit hyperactivity disorder; CI, confidence interval; CNS, central nervous system; IADL, instrumental activities of daily living; ICD-10, international classification of diseases-10th edition; MH, mental health; SSRI, selective serotonin reuptake inhibitor

1. Introduction

Climate change is a critical determinant of human health and is increasingly recognized for its impact on mental well-being [1]. While mental health (MH) is particularly affected [2] and mental disorders become increasingly prevalent worldwide [3], their impacts have only recently begun to receive systematic attention [4].

The psychiatric literature has focused mainly on three of the four context-specific climate-exposures (Fig 1): (i) the existential threat of climate change, which can give rise to climate- or eco-anxiety [5]; (ii) extreme weather events, which may induce trauma or post-traumatic stress via direct (e.g., through the loss of a family member) or indirect (e.g., via financial insecurity) pathways [2,6]; and (iii) air pollution, associated with oxidative stress, systemic inflammation, neuroinflammation, and altered brain function [7]. In contrast, the effects of (iv) heat remain relatively underexplored, particularly regarding its underlying mechanisms and disorder-specific outcomes [8].

thumbnail
Download:
Fig 1. The distinct pathways through which climate change impacts MH: climate change in general, extreme weather events, heat, and air pollution.

Source: authors.

https://doi.org/10.1371/journal.pclm.0000958.g001

Existing evidence indicates that elevated ambient temperature - in this review referred to as acute thermal stress rather than chronic gradual warming - increases the risk of psychiatric hospitalization [9], emergency visits [10], ambulance dispatches [11], and mortality [12,13]. One meta-analysis found that for each 1 °C increase in temperature, the relative risk for MH-related mortality and morbidity rose by 2.2% (confidence interval (CI) 95% 1.015;1.029) and 0.9% (CI 95% 1.007;1.015), respectively [14]. Numerous studies have associated heat with negative outcomes in six MH subgroups [2,4,6,12,14]: suicidal behaviour [15], schizophrenia [9], substance misuse [16], bipolar [17], organic [18], and neurotic disorders [13]. Additional MH disorders were also identified as heat-sensitive in the literature, however, less consistently [2,4,6,12,14], as follows: depressive disorders, behavioural disorders, intellectual disabilities, developmental disorders (e.g., autism spectrum), and behavioural and emotional disorders with onset in childhood or adolescence (e.g., attention deficit hyperactivity disorder (ADHD)).

An open question in the field is whether heat can directly precipitate new-onset MH disorders. A study reported a correlation between higher annual average temperatures and increased incidence of depression [19]. Likewise, a cohort study in Taiwan found that individuals with prior heat-related illnesses had a higher risk of developing psychiatric disorders [20]. The authors suggest that a possible mechanism might be directly linked to heat-induced brain damage resulting from acute thermal stress. Notably, animal studies found cognitive dysfunction, neuronal damage, degeneration, apoptosis, and amyloid plaque in the hippocampus [20]. These findings, though preliminary, suggest a potentially novel pathway by which climate change could increase the incidence - not only the severity - of mental illness. However, current evidence remains limited, and to our knowledge, no additional studies have confirmed a causal link between heat exposure and the onset of psychiatric disorders. Given this gap, the current narrative review examines how heat impacts individuals with pre-existing disorders.

Two reviews published in 2018 [21] and 2025 [22] have previously examined the mechanisms linking heat exposure and patients with pre-existing MH. Both provided valuable overviews of potential general physiological (e.g., inflammatory responses), psychological (e.g., health anxiety), behavioural (e.g., sleep disruption), and social pathways (e.g., social isolation). However, they did not examine (i) pathophysiological disease-specific pathways - for example, why individuals with schizophrenia or bipolar disorder appear particularly vulnerable - even though not all disorders share the same level of susceptibility or underlying mechanisms. Besides, they did not integrate (ii) the dual typology of clinical outcomes resulting from heat exposure: the exacerbation of pre-existing mental disorders and/or the onset of heat-related illnesses. This gap aligns with prior research emphasizing the importance of healthcare professionals recognizing the broad range of clinical presentations associated with heat and MH [23]. Moreover, these reviews lacked detailed guidance on adaptation strategies tailored to the needs of different societal stakeholders. This lack of specificity poses several challenges: it limits patients and caregivers in adopting disorder-specific protective behaviours; it constrains clinicians in identifying and managing heat-related cases based on underlying pathophysiological mechanisms; it impedes researchers in designing focused, mechanism-oriented studies; and it delays the development of targeted public health interventions by policymakers. In response to these challenges, the World Health Organization has underscored the importance of deepening our understanding of the mechanisms connecting heat exposure and MH to inform both mitigation and adaptation efforts [24].

This study was conducted as a narrative review, which differs in nature from a scoping or systematic review, particularly in its methodology. It aims to synthesize the literature on the topic, critically interpret the evidence, and offer novel perspectives based on current knowledge. Moreover, it does not follow a strict research protocol (e.g., PRISMA [25]) as required for systematic or scoping literature reviews, allowing for a flexible, subjective approach. Given the lack of experimental studies in the field, we build on existing research to propose new perspectives on 1) disease-specific mechanisms and 2) the dual clinical outcomes of heat exposure on MH—namely, symptom exacerbation and the onset of heat-related illnesses. Our goal is to promote new conceptual understanding and inform targeted interventions at both clinical and policy levels, thereby supporting broader efforts to address the intersecting challenges of rising global temperatures and the growing burden of MH disorders.

Search strategy

A literature search was conducted in MEDLINE (via PubMed) and Google Scholar between January 2023 and September 2025. We also performed backward citation tracking of relevant reviews and primary studies. No restrictions were placed on publication language, date or article type, although priority was given to peer-reviewed original research and reviews that directly addressed mechanisms or clinical outcomes. The keywords used for the databases search were: ‘climate change’, ‘heat’, ‘extreme heat’, ‘heatwave,’ ‘mechanism’, ‘exacerbation’, ‘heat-related illness’, ‘mental health’, ‘psychiatric disorder’, ‘organic disorder’, ‘dementia’, ‘substance misuse’, ‘substance abuse’, ‘alcohol abuse’, ‘drug abuse’, ‘schizophrenia’, ‘mood disorder’, ‘depression’, ‘depressive disorder’, ‘mood disorder’, ‘bipolar disorder’, ‘neurotic disorder’, ‘anxiety disorder’, ‘behavioural disorder’, ‘intellectual disability’, ‘developmental disorder’, ‘autism’, ‘attention deficit hyperactivity disorder’, ‘ADHD’.

Inclusion and synthesis

Studies were included if they addressed either (i) mechanisms by which heat affects mental health or (ii) clinical outcomes related to heat exposure to psychiatric disorders. Article screening and quality appraisal were conducted iteratively by the authors, who selected studies based on relevance to the research questions. Findings were then thematically synthesized to identify shared and disorder-specific mechanisms and outcomes.

2. The effects of heat on the human body: Adequate thermoregulation

Understanding adequate thermoregulatory responses might contribute to a more robust comprehension of the disrupted mechanisms underlying MH conditions. First, as illustrated in Fig 2, once exposed to heat, one must accurately perceive it to trigger appropriate thermoregulatory responses [26]. Further, heat stimuli are then received (through skin thermoreceptors)and transmitted from the peripheral nervous system to the central nervous system (CNS), where signals are processed by the hypothalamus. This step requires intact sensory integration and cognitive functioning (e.g., attention, executive control) to recognize stressors and initiate adequate responses [27].

thumbnail
Download:
Fig 2. Graphical representation of the thermoregulation process in the human body under extreme heat exposure.

The first phase involves heat exposure itself, followed by the reception, transmission, and processing of thermal stimuli. The third phase consists of the physiological responses mediated by the somatic (voluntary) and autonomic (involuntary) nervous systems. Disruption of any of these phases by factors such as MH disorders or certain medications may lead to heat-related illnesses, characterized by impaired heat dissipation and a consequent rise in core body temperature. Source: authors. Icons from OpenClipart.org (Public Domain).

https://doi.org/10.1371/journal.pclm.0000958.g002

In response, the hypothalamus activates two complementary pathways. The somatic nervous system (voluntary control) enables behavioural thermoregulation - actions such as seeking shade or cooler environments, removing excess clothing, increasing fluid intake, and reducing unnecessary physical activity, especially at work, to minimize internal heat production [26,28].

Additionally, the hypothalamus engages the autonomic nervous system (involuntary control). Through complex neurotransmitter signalling (e.g., acetylcholine, dopamine, serotonin), this system triggers physiological thermoregulatory mechanisms including: radiation (heat dissipation through vasodilation of skin capillaries, responsible for approximately 60% of heat loss), evaporation (sweating and respiratory heat loss, contributing to around 20% of heat loss), conduction (direct heat transfer from warmer to cooler surfaces), and convection (heat flow from the body to the surrounding air, enhanced by wind or fans) [26,28]. The last two mechanisms account for relatively less heat dissipation.

If these mechanisms fail to dissipate sufficient heat and no additional interventions are implemented, core body temperature may continue to rise, potentially leading to hyperthermia and associated heat-related illnesses. While any individual exposed to extreme heat may be affected, vulnerable populations - e.g., patients with schizophrenia or organic disorders - are at greater risk for developing a heat-related illness, as further presented in this review.

3. The dual effect of heat on mental health

The body of literature indicates that heat has a twofold impact on individuals with MH disorders. This conclusion is based on direct evidence from existing studies, combined with a critical review of disease-specific pathways. Where direct evidence linking heat exposure to specific psychiatric outcomes was limited, pathways were built through systematic reasoning across established disease-specific physiology (e.g., dopamine hypothesis of schizophrenia), pharmacological mechanisms (e.g., anticholinergic effects), and validated psychological frameworks (e.g., vulnerability-stress model). This approach was necessary given the emerging state of the primary literature in this field. Fig 3 synthesizes these findings, and the subsequent sections present a more detailed breakdown of the results. On the left, heat exposure can lead to a) heat-related illnesses, affecting mostly patients with organic disorders, substance misuse, and schizophrenia, as confirmed by a paper investigating heat-related illnesses in patients with MH disorders [29]. This likely occurs through three broad pathways: cognitive impairment, disease-related neural dysfunction, and the influence of substances or medications. While on the right, heat can b) exacerbate pre-existing MH conditions, such as schizophrenia [30], bipolar disorder [31], suicidal behaviour [32], and neurotic disorders [33], through three broad pathways likely involving physiological stress, neurotransmitter imbalance, and sleep disruption.

thumbnail
Download:
Fig 3. Detailed mechanisms linking heat and MH.

Graphical representation of the two pathways through which heat exposure may impact patients with MH disorders, leading to heat-related illnesses and/or exacerbation of pre-existing disorders. Source: authors, based on the body of evidence gathered in this review.

https://doi.org/10.1371/journal.pclm.0000958.g003

a. Heat-related illness

A heat-related illness is characterized by an increase in core body temperature leading to heat exhaustion, heat stroke - a health emergency, when the temperature reaches 40 °C -, or to mortality [34].

i. Ineffective thermoregulatory behaviours linked to cognitive impairment.

As discussed above, thermoregulatory behaviours are important for effective heat dissipation. However, cognitive impairment associated with specific MH disorders may hinder effective behavioural adaptation, e.g., appropriate hydration, clothing adaptation, and seeking shaded areas [22,35]. Moreover, patients might engage in physical movements, such as wandering or maintaining strong muscle contraction, which can, in turn, increase internal heat production and elevate core temperature [36].

ii. Disease-related impaired neuropathways affecting thermoregulation.

The hypothalamus regulates core temperature through fine neurotransmitter responses, e.g., serotonin [37], dopamine [38,39], and noradrenaline [40]. In this context, specific MH disorders seem to be related to an intrinsic neurotransmitter imbalance, which, in turn, might affect thermoregulatory responses. Namely, for instance, the first and one of the most established theories behind schizophrenia is explained by an abnormal dopamine activity in the CNS, likely hindering effective heat regulation via the hypothalamus [41]. This intercorrelation potentially explains the higher core body temperature among patients with schizophrenia when compared to healthy controls, which was shown during one of the few experiments carried out in the context [42].

iii. Use of substances, e.g., alcohol or drugs, and intake of specific psychotropic medications.

Psychoactive substances impose behavioural, physiological, and psychological effects that might impact the thermoregulatory process [40]. Such substances might have different impacts on the thermoregulation phases, e.g., affecting awareness, increasing exposure to heat, and hampering somatic and autonomic nervous system responses [26,43].

Specifically, psychotropic medications might influence body temperature maintenance by modulating neuropathways, particularly those linked to the cholinergic system, which is responsible for activating sweat glands and vasodilation [44–46]. Moreover, polypharmacy, common in severe mental disorders, can intensify thermoregulatory impairment, particularly when multiple medications interact to alter autonomic responses. Older adults and frail patients are at additional risk due to reduced physiological reserve and impaired behavioural responses [47].

Particularly, antipsychotics, opioids, hypnotics, anxiolytics, and antiparkinsonian agents have all been associated with significant heat intolerance [44–46], and the World Health Organization identifies these drugs as contributors to elevated core body temperature during heat stress [48]. Table 1 delineates the specific medication classes and their potential mechanisms for impacting heat dissipation.

thumbnail
Download:
Table 1. Thermoregulatory dysfunction associated with commonly prescribed psychotropic and neurological medications: anticholinergic, dopaminergic, and neuroendocrine mechanisms of heat intolerance. Source: authors, building on the work of Bouchama (2007) [49], the National Centre for Diseases Prevention and Control (2011) and Hajat, O’Connor & Kosatsky (2010) [50].

https://doi.org/10.1371/journal.pclm.0000958.t001

The antipsychotics act on the CNS, more specifically, blocking the dopaminergic pathway. The side effect is that by altering the dopaminergic system, the drug also prevents the patient from efficient hypothalamic temperature regulation. Besides, they also block the cholinergic pathway and reduce sweating and vasodilation [40]. The opiates influence the skin vasculature and prevent the patient from properly sweating. Hypnotics and anxiolytics are well known for depressing the CNS, and, as a side effect, they cause significant dehydration, which is worse when combined with heat exposure. Lastly, antiparkinsonians are anticholinergic drugs, like antipsychotics, so they have similar effects on heat dissipation [40].

Despite not being as consistently reported in the literature [51], antidepressants seem to increase the risk of impaired heat dissipation to a certain extent through various pathways of action in the body [43]. For example, the ‘selective serotonin reuptake inhibitor’ (SSRI) class of antidepressant, mainly represented by fluoxetine or escitalopram, increases the final serotonin levels in the body, and if in high doses - amplified by heat exposure -, may lead to serotonin syndrome, characterized by hyperthermia and higher heat production, hypertension, and tachycardia [52]. Moreover, classes such as dopamine/norepinephrine reuptake inhibitors were associated with higher core body and lower peripheral temperature in rats, suggesting reduced capacity of heat dissipation [53].

Nevertheless, the difficulty in untangling the medication from the MH disorder being treated (e.g., schizophrenia [34]) requires further epidemiological studies testing more drugs and aiming to better understand their effects. S1 Table in the supplementary materials provides a detailed overview of drug classes and their respective medications, followed by the likelihood of heat sensitivity. The effect of other drugs is specifically discussed in the section ‘substance misuse’ below.

b. Exacerbation of pre-existing MH disorders

Disease exacerbation is characterized by deterioration in disease control and subsequent symptom onset. The seasonality reported in some MH diseases, such as bipolar disorders [54], already indicates that environmental factors play a role in disease patterns. The specific pathways in this context are delineated below, as follows:

i. Heat as a physiological stressor.

Studies have already shown that heat exposure acts as a physiological stressor, activating the hypothalamic-pituitary-adrenal (HPA) axis and triggering the inflammatory cascade [55,56]. Consequently, inflammatory markers (e.g., interleukin-1β, glial fibrillary acid protein, tumor necrosis factor α, etc.), neurotransmitters, and hormones are released [55,56], potentially unfolding emotional and physiological alterations, e.g., concentration, emotion, and cognition impairment [57]. In generally healthy populations with significant physiological and emotional reserve, such stressors might have only limited outcomes [57]. However, the vulnerability–stress model - a well-established psychological framework - emphasizes that, for individuals with MH disorders, even minor fluctuations in stress can lead to disproportionately pronounced outcomes [57]. The model presents that the onset or exacerbation of a MH disorder depends not only on pre-existing vulnerabilities (e.g., genetic predispositions or early-life trauma) but also on the presence of an acute stressor capable of precipitating symptom expression. Within this context, the theory suggests that individuals with MH disorders reach their stress tolerance threshold more readily [57]. As a result, the same environmental temperature may elicit markedly different stress responses across individuals, potentially leading to acute symptom exacerbations in vulnerable populations.

ii. Hormones and neurotransmitter imbalance.

Exposure to heat [58] and light [59] has been linked to disruptions in hormones and neurotransmitters, such as serotonin, adrenaline, noradrenaline, and cortisol. These alterations appear to contribute to mood changes and may exacerbate acute symptoms in individuals with MH disorders, who are particularly susceptible to such physiological fluctuations [60]. Acute psychiatric symptoms (e.g., aggressivity [61] and impulsivity [62] among patients at high risk for suicidal behaviour) are closely tied to specific neural pathways within the central nervous system. Evidence indicates that these neurochemicals regulate fundamental emotional states, including joy, anger, and sadness [63]. Consequently, environmentally induced disturbances in neurochemical balance may substantially affect the stability and clinical management of MH conditions.

iii. Sleep disruption.

Elevated ambient temperature is among the most important environmental factors affecting sleep [64]. Previous studies have reported that heat leads to worse sleep quality and shorter duration [22,65], by increasing wakefulness [66] and decreasing important consolidation and restorative phases [67]. In turn, appropriate sleep quality and duration play a critical regulatory role in brain functions, emotion regulation, and overall psychological resilience [68]. For example, sleep helps regulate serotonin, dopamine, and epinephrine [69]. Likewise, disrupted sleep patterns can increase pro-inflammatory markers [70,71] and cortisol levels, and impair emotion regulation, heightening emotional reactivity and reducing the ability to regulate stress [69]. Therefore, the sleep disruption directly linked to heat-related discomfort seems to contribute to the worsening of symptoms and exacerbation of chronic MH conditions, e.g., for Parkinson’s disease [72] and bipolar disorder [73].

4. Disease-specific pathways for heat sensitivity

The following sections integrate the dual outcomes explored above into the disease-specific pathways through which heat affects MH.

i. Organic disorders

A meta-analysis of 3 studies published in 2021 found that each 1 °C rise in temperature was associated with a mortality-related relative risk of 1.033 (CI 1.020; 1.046) [14], while a study in Vietnam showed that a 7-day heatwave was associated with a relative risk of hospitalization of 3.62 (CI 1.76; 7.42) [74]. Gong and colleagues (2022) still projected that, under a high-emissions scenario, heat-related admissions could increase by 300% in England by 2040 [18].

As shown by primary research [29] and due to the characteristics of organic disorders, patients are especially likely to exhibit increased vulnerability to heat-related illness as the main outcome [18,21,75]. This vulnerability seems to rely primarily on the inefficient thermoregulatory behaviours. In advanced stages, such diseases may reduce the patient’s mobility, leading, for example, to reduced fluid intake [49,47].

Besides, patients diagnosed with dementia are mainly elderly, who are naturally more vulnerable to heat. At advanced ages, the delay and impairment of heat regulation are anatomically explained, as both the receptor system and the thermoregulatory neural areas become less efficient over time [76]. Moreover, peripheral nerve fibers and receptors limit heat sensibility, sweat glands are less efficient, and the skin is thinner, which prevents proper heat exchange [26].

Notably, evidence shows that, in older adults, greater exposure to extreme heat is linked to significant impairment in performing instrumental activities of daily living (IADL) – a proxy for independent living and effective daily management [77]. Finally, patients with MH disorders, as well as the elderly population, are more likely to be socially isolated or live in nursing homes, which has been proven to increase the risk of heat stress [43,77].

ii. Substance misuse

Heat exposure (28 vs. 19.4 °C) was associated with an increased relative risk of hospitalization due to substance misuse in Hong Kong (1.13, CI 1.00-1.27) [16]. Consistent results were found in South Korea, with a 7% higher mortality risk per 1 °C increase in temperature (1.07, CI 1.02-1.13) [78].

Given the physiological, social, and psychological effects of psychoactive substances described in section a(iii) - and corroborated by a primary study [29] - individuals who misuse such substances potentially exhibit heightened vulnerability to heat-related illness [79]. More specifically, individuals who excessively consume alcohol or other CNS depressants may experience reduced vigilance and cognitive impairment [43], both of which can limit their ability to recognize or appropriately respond to heat stress. Furthermore, alcohol has an important diuretic effect, leading to a significant fluid loss [40,43]. The substance also causes persistent cutaneous vasodilation, which initially helps dissipate heat but ultimately increases fluid evaporation, thereby worsening dehydration [40,43,80]. As dehydration progresses, the body’s capacity to dissipate heat declines, leading to rising core temperatures.

Conversely, sympathomimetic drugs [51], such as cocaine and methylenedioxymethamphetamine (MDMA), stimulate a substantial adrenaline release, increasing metabolic heat production and further contributing to the risk of heat-related illness [40,43].

iii. Schizophrenia

A study in China found a higher relative risk (1.38, CI 1.26; 1.69) of heat (99th percentile of mean temperature against the local minimum risk temperature) on schizophrenia-related hospitalization [81]. These results aligned with a meta-analysis of 7 studies, which found that for each 1 °C increase in temperature, there was a relative risk of 1.007 (CI 1.002; 1.011) of schizophrenia-related morbidity (hospitalization, emergency visits etc.) [14].

Schizophrenia has already been directly associated both with heat-related illness [29] and with exacerbation of disease symptoms [30]. Regarding the first outcome, patients appear to have difficulty efficiently transferring heat from the core to the periphery, thereby increasing their risk of heat-related illness [34]. In an experimental study comparing men diagnosed with schizophrenia who were undergoing antipsychotic treatment with non-affected control participants, individuals with schizophrenia exhibited lower peripheral temperatures throughout most of a heat-tolerance test and a higher core temperature at its conclusion. This pattern suggests an impaired ability to dissipate heat peripherally and to maintain thermoregulatory stability relative to controls.

Mechanistically, dopamine—whose dysregulation is central to the dopaminergic hypothesis of schizophrenia—is also critically involved in hypothalamic temperature regulation (see section a(ii)) [38]. The authors noted, however, that it remains unclear whether the observed thermoregulatory impairment arises from schizophrenia-related neurobiological alterations, from the effects of antipsychotic medications, or from an interaction between the two [34,43].

Additionally, episodes of symptom exacerbation tend to increase when patients are exposed to warmer-than-average temperatures [81]. This outcome might be partly explained by the heightened sensitivity to stress commonly observed in this population, including heat-induced stress. This interpretation aligns with the vulnerability–stress model discussed in section b(i) [82].

iv. Bipolar disorders

A study in Italy reported that emergency admissions due to bipolar disorders were predicted by maximum temperature and solar radiation [83]. In this context, other research performed in Hong Kong found that heat exposure (28 vs. 19.4 °C) was associated with increased relative risks of hospitalization (1.34, CI 1.05; 1.71) [16].

Most of the related studies directly report heat-induced exacerbation of bipolar disorder [31,36,54,60,84]. In particular, literature has consistently demonstrated an increase in manic episodes - a subtype of euphoric and acute phase of bipolar disorder - during early spring, underscoring the disorder’s sensitivity to climatic factors [31,54,85,86]. Notably, cases tend to rise significantly across early spring and summer [54], and one study showed that increases in ambient temperatures were consistently associated with a 0.4% rise in manic symptom scores [87]. Evidence suggests that the rapid and intense increase in sunlight during early spring, the longer daylight hours in warmer seasons, and heat exposure may underlie this association (see section b(ii)) [42,54,60,83]. These environmental factors may increase serotonin turnover in the brain and alter receptor responsiveness, leading to elevated serotonin levels in the CNS, thereby exacerbating manic symptoms [54,59]. Additional neurotransmitter-related mechanisms may involve heat-induced increases in dopamine activity [88] and changes in melatonin secretion driven by light exposure [36,54,84]. Since both melatonin release and heat exposure impact sleep, sleep disturbances have also been linked to the onset of acute symptoms [89].

Conversely, although no studies have directly demonstrated an increased risk of heat-related illness in patients with bipolar disorder, psychotropic medications (e.g., antipsychotics and mood stabilizers) may impair thermoregulatory function. Moreover, from an indirect perspective, individuals with severe mental illnesses—including bipolar disorder—exhibit higher rates of metabolic syndrome [90], a group of conditions that elevate the risk of cardiovascular disease, stroke, and type 2 diabetes. Metabolic syndrome, in turn, is associated with reduced heat tolerance and an increased risk of heat-related illness [91].

v. Suicidal behaviour

An extensive body of literature indicates a clear causal relationship between heat and interpersonal violence, leading to higher risks of homicide [92], domestic violence [93], and assault [94], amongst others. Moreover, heat was also reported to intensify self-violence, directly linked to suicidal behaviour [11]. Burke and colleagues found, in 2018, that suicide rates increased by 0.7% in the United States and 2.1% in Mexico for 1°C of monthly average temperature increase during 1990–2010 [95]. These results are consistent in other countries, e.g., in Brazil [96] and Switzerland [97].

Given that suicide attempts constitute an acute psychiatric event rather than a heat-related illness, as directly confirmed by the studies above, they are classified in the present review within the “exacerbation of pre-existing disorders” subgroup.

The serotonin system represents a key mechanism in the link between impulsive or violent behaviour and suicide. Previous research indicates that increased exposure to heat and light can enhance the responsiveness of serotonin receptors, potentially leading to more aggression and impulsivity [61,62]. Such changes in behaviour may, in turn, contribute to the progression from suicidal thoughts to suicidal actions [36,97]. A study still found that patients with a history of multiple suicide attempts face a higher risk of new self-harm episodes during heat exposure compared to first-time attempters, suggesting that certain pre-existing traits - such as those related to the serotonin system - may consistently heighten vulnerability to heat [98].

vi. Anxiety disorders

Previous papers found that heat increased the risk for healthcare use due to neurotic disorders, mostly anxiety. Heat in Brazil (99th vs. 50th percentile of mean temperature) was associated with a relative risk of emergency visits of 1.18 (CI 1.05; 1.32) [13], while a study in Canada found a relative risk of emergency visits of 1.12 (CI 1.00; 1.27) after heat exposure (99th vs. 50th percentile of mean temperature) [99].

Results from primary studies [33], along with the underlying disease’s pathophysiology, suggest they may be particularly vulnerable to symptom exacerbation. The literature indicates that heat can adversely affect individuals with anxiety disorders, potentially through underlying mechanisms in which heat exposure elevates cortisol and adrenaline levels, thereby exacerbating anxiety-related physiological responses. For example, a recent study demonstrated that patients exhibited an important elevation in anxiety levels following a 1.5-hour heat exposure protocol [33]. The authors attributed this response to heat-induced activation of the systemic inflammatory cascade [33], which can subsequently elevate cortisol [100] and adrenaline levels [58]. Such neuroendocrine changes may further heighten vulnerability to acute symptom worsening in this population.

5. Discussion

This narrative review synthesizes literature and provides a more integrated understanding of the mechanisms linking heat exposure to MH outcomes. Unlike previous reviews that broadly categorized pathways as physical, psychological, social, or behavioural, our analysis adopts a disorder- and outcome-specific lens. The resulting framework has direct implications for clinical practice, public health interventions, and policy design. This review also aligns with previous research recommendations. Crandon and colleagues [23] highlighted the importance of healthcare professionals’ awareness of the range of possible clinical presentations during hot periods.

Clinical implications

This integrated perspective may draw attention from healthcare providers and, by including heat as a risk factor in clinical practice, enhance earlier recognition of heat-related illnesses and prodromal signs of disease exacerbation.

In the longitudinal care, clinicians could counsel high-risk patients - particularly those within the six subgroups identified above - and their caregivers about preventive measures and the early symptoms that warrant urgent evaluation during heat stress. As with other routine risk-factor counseling (e.g., promoting physical activity or limiting sugar intake), heat exposure could be addressed systematically. MH professionals, in particular, play an important role as climate communicators, guiding patients, families, and caregivers toward adaptive strategies. These include reducing heat production (e.g., by discouraging wandering), minimizing heat exposure (e.g., by ensuring access to shaded areas in nursing homes or psychiatric hospitals), and enhancing heat dissipation (e.g., by encouraging adequate hydration and avoiding substances such as alcohol or illicit drugs).

Additionally, in emergency care during the warmest seasons, facilities may consider adapting their existing protocols and guidelines to better stratify and target higher-risk disease subgroups. This risk stratification can be understood through the lens of the vulnerability-stress model, which underscores additional covariates that influence risk, including advanced age [47], reduced mobility [35], comorbidities [101], and medication use [102], among others. Such a protocol could, where feasible, include the systematic assessment of signs of heat exhaustion in vulnerable MH subgroups. Moreover, the patient’s medication list should be more actively assessed during early screening to identify any that might impair heat dissipation and thereby cause a heat-related illness. The Centers for Disease Control and Prevention (CDC, 2025) [103] indicates that clinicians may carefully and individually evaluate whether to adjust dosages or frequencies during warmer months, taking into account the potential risks and benefits. Likewise, once prescribing new medications, MH providers could assess their potential impact on thermoregulation and, if possible, consider safer alternatives with lower risk profiles. Additionally, reassessing fluid restrictions for patients taking medications that may contribute to fluid loss could help prevent dehydration.

Policy implications

Broader-level adaptation measures could also be implemented by policymakers. For instance, investing in climate-resilient healthcare systems would enhance the capacity of health services to anticipate, prevent, absorb, and adapt to upcoming heat events [104]. One widely accepted adaptation strategy is the ‘heatwave early warning system’, a mechanism designed to trigger rapid healthcare responses during periods of extreme heat. During these alert periods, primary healthcare professionals could proactively identify high-risk MH patients - using existing population registries or medical records - and reach out to provide preventive guidance or acute care when necessary.

Similar strategies are already widely implemented to prevent exacerbations of prevalent chronic conditions (e.g., hypertension and diabetes) or to promote vaccination campaigns, particularly in countries with strong primary healthcare systems, such as Brazil and Costa Rica. Consequently, in similar settings, integrating heat exposure as a recognized risk factor for MH conditions would require only an extension of existing preventive frameworks. In addition, such proactive outreach may help reduce healthcare access barriers that discourage patients from seeking care in health facilities during periods of extreme heat [105].

Other practical policy adaptations include enhancing cooling systems in mental healthcare facilities to minimize heat exposure and facilitate heat dissipation among patients [106]. Likewise, the greening of cities and intensive use of green (and blue) spaces have both the potential to minimize heat exposure as well as cortisol levels (see section b(ii)), directly targeting stress-related MH pathways [107]. While certain pharmaceutical companies have already incorporated recommendations concerning the side effects of extreme heat exposure within their package inserts, others have yet to undertake such measures. Medication users would benefit from the systematic inclusion of this information in the package inserts. Lastly and more broadly, the integration of climate change into the curricula of medical students and early career psychiatrists would leverage a more transformative agenda on the topic.

Limitations and future research

Although narrative reviews are useful for providing context, generating hypotheses, offering novel perspectives on a topic and providing a broad overview, they also have limitations, primarily due to the lack of systematic methodology and limited reproducibility. Given the absence of a structured search protocol, it is possible that relevant studies were unintentionally omitted. Nevertheless, we made efforts to minimize bias, included as many sources as possible, and conducted an extensive literature review. Still, the search process was not exhaustive, and the review remains inherently interpretive.

Socioeconomic and environmental determinants, such as work and housing conditions [105] or climate-related stressors (forced migration) [108], can significantly modulate individual vulnerability to heat exposure and subsequent MH outcomes. While these social aspects were not the primary focus of this review, their relevance is acknowledged.

Moreover, our analysis focused exclusively on the mechanisms associated with the most studied and well-established disease subgroups. This does not, however, imply that other conditions are not heat-sensitive or a lack of awareness in this regard. In fact, disorders such as depression [109] and ADHD [110] have been previously linked to increased heat vulnerability. Still, the evidence is inconsistent, and the underlying pathophysiological mechanisms remain incompletely understood. Some potential pathways may range from medication use to physiological mechanisms, which could lead to disease exacerbation or heat-related illness in both conditions. Notably, it is well-known that both disorders usually require different psychotropic medications for proper treatment that might increase heat sensitivity (see section a(iii)), even though part of the potential negative outcomes seem to be attributed to the pre-existing diseases themselves rather than exclusively to the drug effect. A study from 2024 found that patients under stimulant treatment had a lower risk of heat-related illness compared to those with no treatment [111]. Furthermore, an underlying inflammatory aspect was reported for both ADHD [112] and depressive disorders [113], which could be amplified by heat exposure. Nonetheless, given the persisting literature gaps, we recommend conducting a dedicated scoping review on these highly prevalent conditions.

Finally, we found very few studies examining whether, and in what ways, heat exposure directly contributes to the onset of new MH diagnoses. Addressing this research gap is highly encouraged, as exploring this question could substantially enhance our understanding of how rising temperatures may increase the global burden of MH disorders.

6. Conclusion

This narrative review advances the current understanding of how heat exposure affects MH by integrating fragmented evidence into an outcome- and disorder-specific framework. Focusing on the pathophysiological mechanisms underlying heat-related illnesses and the exacerbation of pre-existing psychiatric conditions, the review highlights the six MH subgroups most consistently identified as heat-sensitive. By emphasizing these mechanisms, it offers a basis for early recognition and physiologically informed adaptation strategies. The insights presented here can inform targeted interventions for clinicians, caregivers, and patients, as well as policy measures to reduce the health burden associated with rising temperatures. Collectively, these contributions support the development of a climate-resilient MH system.

Supporting information

S1 Table. Detailed listing of psychotropic medications and their heat sensitivity.

https://doi.org/10.1371/journal.pclm.0000958.s001

(DOCX)

References

  1. 1. Intergovernmental Panel on Climate Change IPCC. Climate Change 2022 – Impacts, Adaptation and Vulnerability. Contribution of Working Group II to the Sixth Assessment Report of the Intergovernmental Panel on Climate Change. Cambridge University Press; 2022. https://doi.org/10.1017/9781009325844
    • 2. Cianconi P, Betrò S, Janiri L. The impact of climate change on mental health: a systematic descriptive review. Front Psychiatry. 2020;11:74. pmid:32210846
    • 3. Dattani S. How are mental illnesses defined? 2023.
      • 4. Charlson FJ, Ali S, Benmarhnia T. Climate change and mental health: a scoping review. Eur J Psychotraumatol. 2022;13(1):1–16.
      • 5. Brophy H, Olson J, Paul P. Eco-anxiety in youth: an integrative literature review. Int J Ment Health Nurs. 2023;32(3):633–61. pmid:36582129
      • 6. Corvetto JF, Helou AY, Dambach P, Müller T, Sauerborn R. A systematic literature review of the impact of climate change on the global demand for psychiatric services. 2023. pp. 1–26.
        • 7. Braithwaite I, Zhang S, Kirkbride JB, Osborn DPJ, Hayes JF. Air pollution (particulate matter) exposure and associations with depression, anxiety, bipolar, psychosis and suicide risk: A systematic review and meta-analysis. 2019;127.
          • 8. Berrang-Ford L, Sietsma AJ, Callaghan M, Minx JC, Scheelbeek PFD, Haddaway NR, et al. Systematic mapping of global research on climate and health: a machine learning review. Lancet Planet Health. 2021;5(8):e514–25. pmid:34270917
          • 9. Dang TN, Vy NTT, Thuong DTH, Phung D, Van Dung D, Le An P. Main and added effects of heatwaves on hospitalizations for mental and behavioral disorders in a tropical megacity of Vietnam. Environ Sci Pollut Res Int. 2022;29(39):59094–103. pmid:35378653
          • 10. Nori-Sarma A, Sun S, Sun Y, Spangler KR, Oblath R, Galea S, et al. Association between ambient heat and risk of emergency department visits for mental health among US adults, 2010 to 2019. JAMA Psychiatry. 2022;79(4):341–9. pmid:35195664
          • 11. Kubo R, Ueda K, Seposo X, Honda A, Takano H. Association between ambient temperature and intentional injuries: A case-crossover analysis using ambulance transport records in Japan. Sci Total Environ. 2021;774:145511. pmid:33609821
          • 12. Thompson R, Hornigold R, Page L, Waite T. Associations between high ambient temperatures and heat waves with mental health outcomes: a systematic review. Public Health. 2018;161:171–91. pmid:30007545
          • 13. Corvetto JF, Federspiel A, Sewe MO, Müller T, Bunker A, Sauerborn R. Impact of heat on mental health emergency visits: a time series study from all public emergency centres, in Curitiba, Brazil. BMJ Open. 2023;13(12):e079049. pmid:38135317
          • 14. Liu J, Varghese BM, Hansen A, Xiang J, Zhang Y, Dear K, et al. Is there an association between hot weather and poor mental health outcomes? A systematic review and meta-analysis. Environ Int. 2021;153:106533. pmid:33799230
          • 15. Pan R, Honda Y, Minakuchi E, Kim SE, Hashizume M, Kim Y. Ambient temperature and external causes of death in Japan from 1979 to 2015: a time-stratified case-crossover analysis. Environ Health Perspect. 2022;130(4):47004. pmid:35394808
          • 16. Chan EYY, Lam HCY, So SHW, Goggins WB, Ho JY, Liu S, et al. Association between Ambient Temperatures and Mental Disorder Hospitalizations in a Subtropical City: a time-series study of Hong Kong Special Administrative Region. Int J Environ Res Public Health. 2018;15(4):754. pmid:29662001
          • 17. Zhang S, Yang Y, Xie X, Li H, Han R, Hou J, et al. The effect of temperature on cause-specific mental disorders in three subtropical cities: a case-crossover study in China. Environ Int. 2020;143:105938. pmid:32688157
          • 18. Gong J, Part C, Hajat S. Current and future burdens of heat-related dementia hospital admissions in England. Environ Int. 2022;159:107027. pmid:34890899
          • 19. Chen N-T, Lin P-H, Guo Y-LL. Long-term exposure to high temperature associated with the incidence of major depressive disorder. Sci Total Environ. 2019;659:1016–20. pmid:31096317
          • 20. Kuo W-Y, Huang C-C, Chen C-A, Ho C-H, Tang L-Y, Lin H-J, et al. Heat-related illness and dementia: a study integrating epidemiological and experimental evidence. Alzheimers Res Ther. 2024;16(1):145. pmid:38961437
          • 21. Lõhmus M. Possible biological mechanisms linking mental health and heat-a contemplative review. Int J Environ Res Public Health. 2018;15(7):1515. pmid:30021956
          • 22. Baecker L, Iyengar U, Del Piccolo MC, Mechelli A. Impacts of extreme heat on mental health: Systematic review and qualitative investigation of the underpinning mechanisms. J Clim Chang Health. 2025;22:100446. pmid:41646246
          • 23. Crandon TJ, Dey C, Scott JG, Thomas HJ, Ali S, Charlson FJ. The clinical implications of climate change for mental health. Nat Hum Behav. 2022;6(11):1474–81. pmid:36385181
          • 24. World Health Organization. Mental health and climate change: policy brief. 2022.
            • 25. Page MJ, Moher D, Bossuyt PM, Boutron I, Hoffmann TC, Mulrow CD, et al. PRISMA 2020 explanation and elaboration: updated guidance and exemplars for reporting systematic reviews. BMJ. 2021;372:n160. pmid:33781993
            • 26. Koop LK, Tadi P. Physiology, heat loss. StatPearls. Treasure Island (FL): StatPearls Publishing; 2024.
              • 27. Kovats RS, Hajat S. Heat stress and public health: a critical review. Annu Rev Public Health. 2008;29:41–55. pmid:18031221
              • 28. Madden CJ, Morrison SF. Central nervous system circuits that control body temperature. Neurosci Lett. 2019;696:225–32. pmid:30586638
              • 29. Schmeltz MT, Gamble JL. Risk characterization of hospitalizations for mental illness and/or behavioral disorders with concurrent heat-related illness. PLoS One. 2017;12(10):e0186509. pmid:29036206
              • 30. Yoon L, Tetzlaff EJ, Chiu T, Wong C, Hiscox L, Choquette D, et al. Surviving the 2021 heat dome with schizophrenia: a qualitative, interview-based unpacking of risks and vulnerabilities. Soc Sci Med. 2025;366:117656. pmid:39740630
              • 31. Medici CR, Vestergaard CH, Hadzi-Pavlovic D, Munk-Jørgensen P, Parker G. The impact of climate on risk of mania. Eur psychiatr. 2016;33(S1):S74–S74.
              • 32. Burke M, González F, Baylis P. Higher temperatures increase suicide rates in the United States and Mexico. https://doi.org/10.1038/s41558-018-0222-x
                • 33. Fang W, Liu L, Yin B, Ke L, Su Y, Liu F, et al. Heat exposure intervention, anxiety level, and multi-omic profiles: a randomized crossover study. Environ Int. 2023;181:108247. pmid:37871510
                • 34. Hermesh H, Shiloh R, Epstein Y, Manaim H, Weizman A, Munitz H. Heat intolerance in patients with chronic schizophrenia maintained with antipsychotic drugs. Am J Psychiatry. 2000;157(8):1327–9. pmid:10910799
                • 35. Kim Y-O, Lee W, Kim H, Cho Y. Social isolation and vulnerability to heatwave-related mortality in the urban elderly population: A time-series multi-community study in Korea. Environ Int. 2020;142:105868. pmid:32593050
                • 36. Volpe FM, Tavares A, Del Porto JA. Seasonality of three dimensions of mania: psychosis, aggression and suicidality. J Affect Disord. 2008;108(1–2):95–100. pmid:18029026
                • 37. Ishiwata T, Hasegawa H, Greenwood BN. Involvement of serotonin in the ventral tegmental area in thermoregulation of freely moving rats. Neurosci Lett. 2017;653:71–7. pmid:28527719
                • 38. Lee TF, Mora F, Myers RD. Dopamine and thermoregulation: an evaluation with special reference to dopaminergic pathways. Neurosci Biobehav Rev. 1985;9(4):589–98. pmid:3001601
                • 39. Scott IM, Boulant JA. Dopamine effects on thermosensitive neurons in hypothalamic tissue slices. Brain Res. 1984;306(1–2):157–63. pmid:6466970
                • 40. Cusack L, de Crespigny C, Athanasos P. Heatwaves and their impact on people with alcohol, drug and mental health conditions: a discussion paper on clinical practice considerations. J Adv Nurs. 2011;67(4):915–22. pmid:21214621
                • 41. Meltzer HY, Stahl SM. The dopamine hypothesis of schizophrenia. Perspect Psychiatr Care. 1990;26(3):18–23.
                • 42. Montes JM, Serrano C, Pascual-Sanchez A. The influence of weather on the course of bipolar disorder: a systematic review. Eur J Psychiatry. 2021;35(4):261–73.
                • 43. Page LA, Hajat S, Kovats RS, Howard LM. Temperature-related deaths in people with psychosis, dementia and substance misuse. Br J Psychiatry. 2012;200(6):485–90. pmid:22661680
                • 44. Stöllberger C, Lutz W, Finsterer J. Heat-related side-effects of neurological and non-neurological medication may increase heatwave fatalities. Eur J Neurol. 2009;16(7):879–82. pmid:19453697
                • 45. Wong AYS, Iwagami M, Taniguchi Y, et al. The role of psychotropics on the associations between extreme temperature and heat-related outcomes among people with mental health conditions: population-based study. 2024.
                  • 46. Kalisch Ellett LM, Pratt NL, Le Blanc VT, Westaway K, Roughead EE. Increased risk of hospital admission for dehydration or heat-related illness after initiation of medicines: a sequence symmetry analysis. J Clin Pharm Ther. 2016;41(5):503–7. pmid:27378245
                  • 47. Bunker A, Wildenhain J, Vandenbergh A, Henschke N, Rocklöv J, Hajat S, et al. Effects of air temperature on climate-sensitive mortality and morbidity outcomes in the elderly; a systematic review and meta-analysis of epidemiological evidence. EBioMedicine. 2016;6:258–68. pmid:27211569
                  • 48. World Health Organization - Regional Office for Europe. Public Health Advice on Preventing Health Effects of Heat: New and Updated Information for Different Audiences. World Health Organization. Regional Office for Europe; 2011.
                    • 49. Bouchama A, Dehbi M, Mohamed G, Matthies F, Shoukri M, Menne B. Prognostic factors in heat wave related deaths: a meta-analysis. Arch Intern Med. 2007;167(20):2170–6. pmid:17698676
                    • 50. Hajat S, O’Connor M, Kosatsky T. Health effects of hot weather: from awareness of risk factors to effective health protection. Lancet. 2010;375(9717):856–63. pmid:20153519
                    • 51. Hospers L, Dillon GA, McLachlan AJ, Alexander LM, Kenney WL, Capon A, et al. The effect of prescription and over-the-counter medications on core temperature in adults during heat stress: a systematic review and meta-analysis. EClinicalMedicine. 2024;77:102886. pmid:39513185
                    • 52. Niu Y, Gao Y, Yang J, Qi L, Xue T, Guo M, et al. Short-term effect of apparent temperature on daily emergency visits for mental and behavioral disorders in Beijing, China: A time-series study. Sci Total Environ. 2020;733:139040. pmid:32446053
                    • 53. Hasegawa H, Meeusen R, Sarre S, Diltoer M, Piacentini MF, Michotte Y. Acute dopamine/norepinephrine reuptake inhibition increases brain and core temperature in rats. J Appl Physiol (1985). 2005;99(4):1397–401. pmid:15920099
                    • 54. Volpe FM, Del Porto JA. Seasonality of admissions for mania in a psychiatric hospital of Belo Horizonte, Brazil. J Affect Disord. 2006;94(1–3):243–8. pmid:16777234
                    • 55. Ovsiannikova Y, Pokhilko D, Kerdyvar V, Krasnokutsky M, Kosolapov O. Peculiarities of the impact of stress on physical and psychological health. Multidiscip Sci J. 2024;6:2024ss0711.
                    • 56. Belity T, Horowitz M, Hoffman JR, Epstein Y, Bruchim Y, Todder D, et al. Heat-stress preconditioning attenuates behavioral responses to psychological stress: the role of HSP-70 in modulating stress responses. Int J Mol Sci. 2022;23(8):4129. pmid:35456946
                    • 57. Walker EF, Diforio D, Walker F. Schizophrenia: a neural diathesis-stress model there have been no integrative analy. Psychol Rev. 1997;104(4):667–85.
                    • 58. McMorris T, Swain J, Smith M, Corbett J, Delves S, Sale C, et al. Heat stress, plasma concentrations of adrenaline, noradrenaline, 5-hydroxytryptamine and cortisol, mood state and cognitive performance. Int J Psychophysiol. 2006;61(2):204–15. pmid:16309771
                    • 59. Lambert GW, Reid C, Kaye DM, Jennings GL, Esler MD. Effect of sunlight and season on serotonin turnover in the brain. Lancet. 2002;360(9348):1840–2. pmid:12480364
                    • 60. Shapira A, Shiloh R, Potchter O, Hermesh H, Popper M, Weizman A. Admission rates of bipolar depressed patients increase during spring/summer and correlate with maximal environmental temperature. Bipolar Disord. 2004;6(1):90–3. pmid:14996147
                    • 61. Sakaue M, Ago Y, Sowa C, Sakamoto Y, Nishihara B, Koyama Y, et al. Modulation by 5-hT2A receptors of aggressive behavior in isolated mice. Jpn J Pharmacol. 2002;89(1):89–92. pmid:12083749
                    • 62. Nomura M, Nomura Y. Psychological, neuroimaging, and biochemical studies on functional association between impulsive behavior and the 5-HT2A receptor gene polymorphism in humans. Ann N Y Acad Sci. 2006;1086:134–43.
                    • 63. Jiang Y, Zou D, Li Y. Monoamine neurotransmitters control basic emotions and affect major depressive disorders. Pharmaceuticals. 2022;15(10).
                    • 64. Chevance G, Minor K, Vielma C, Campi E, O’Callaghan-Gordo C, Basagaña X, et al. A systematic review of ambient heat and sleep in a warming climate. Sleep Med Rev. 2024;75:101915. pmid:38598988
                    • 65. Mullins JT, White C. Temperature and mental health: evidence from the spectrum of mental health outcomes. J Health Econ. 2019;68:102240. pmid:31590065
                    • 66. Okamoto-Mizuno K, Mizuno K. Effects of thermal environment on sleep and circadian rhythm. J Physiol Anthropol. 2012;31(1):14. pmid:22738673
                    • 67. Yuksel C, Denis D, Coleman J, Ren B, Oh A, Cox R, et al. Both slow wave and rapid eye movement sleep contribute to emotional memory consolidation. Commun Biol. 2025;8(1):485. pmid:40123003
                    • 68. Palmer CA, Bower JL, Cho KW, Clementi MA, Lau S, Oosterhoff B, et al. Sleep loss and emotion: a systematic review and meta-analysis of over 50 years of experimental research. Psychol Bull. 2024;150(4):440–63. pmid:38127505
                    • 69. Vaseghi S, Mostafavijabbari A, Alizadeh M-S, Ghaffarzadegan R, Kholghi G, Zarrindast M-R. Intricate role of sleep deprivation in modulating depression: focusing on BDNF, VEGF, serotonin, cortisol, and TNF-α. Metab Brain Dis. 2023;38(1):195–219. pmid:36399239
                    • 70. Krysta K, Krzystanek M, Bratek A, Krupka-Matuszczyk I. Sleep and inflammatory markers in different psychiatric disorders. J Neural Transm (Vienna). 2017;124(Suppl 1):179–86. pmid:26649857
                    • 71. Frey DJ, Fleshner M, Wright KP Jr. The effects of 40 hours of total sleep deprivation on inflammatory markers in healthy young adults. Brain Behav Immun. 2007;21(8):1050–7. pmid:17524614
                    • 72. Mao J, Huang X, Yu J, Chen L, Huang Y, Tang B, et al. Association between REM sleep behavior disorder and cognitive dysfunctions in Parkinson’s disease: a systematic review and meta-analysis of observational studies. Front Neurol. 2020;11:577874. pmid:33240202
                    • 73. Kanady JC, Soehner AM, Klein AB, Harvey AG. The association between insomnia-related sleep disruptions and cognitive dysfunction during the inter-episode phase of bipolar disorder. J Psychiatr Res. 2017;88:80–8. pmid:28088728
                    • 74. Trang PM, Rocklöv J, Giang KB, Kullgren G, Nilsson M. Heatwaves and hospital admissions for mental disorders in Northern Vietnam. PLoS One. 2016;11(5):e0155609. pmid:27195473
                    • 75. Gao Y, Lin L, Yin P, Kan H, Chen R, Zhou M. Heat exposure and dementia-related mortality in China. JAMA Netw Open. 2024;7(6):e2419250. pmid:38941091
                    • 76. Jung D, Kim H, An J, Hong T. Thermoregulatory responses of young and elderly adults under temperature ramps. Build Environ. 2023;244:110760.
                    • 77. Ji H, Shin SH, Coronado A, Lee HY. Extreme heat, functional disability, and social isolation: risk disparity among older adults. J Appl Gerontol. 2025;44(4):561–70. pmid:39287495
                    • 78. Kim CT, Lim YH, Woodward A, Kim H. Heat-attributable deaths between 1992 and 2009 in Seoul, South Korea. PLoS One. 2015;10(2):1–14.
                    • 79. Morris NB, Ravanelli N, Chaseling GK. The effect of alcohol consumption on human physiological and perceptual responses to heat stress: a systematic scoping review. Environ Health. 2024;23(1):73. pmid:39267036
                    • 80. Ciucă Anghel D-M, Nițescu GV, Tiron A-T, Guțu CM, Baconi DL. Understanding the mechanisms of action and effects of drugs of abuse. Molecules. 2023;28(13):4969. pmid:37446631
                    • 81. Pan R, Wang Q, Yi W, Wei Q, Cheng J, Su H. Temporal trends of the association between extreme temperatures and hospitalisations for schizophrenia in Hefei, China from 2005 to 2014. Occup Environ Med. 2021;78(5):364–70. pmid:33737328
                    • 82. Zubin J, Spring B. Vulnerability: a new view of schizophrenia. J Abnorm Psychol. 1977;86(2):103–26.
                    • 83. Aguglia A, Serafini G, Escelsior A, Canepa G, Amore M, Maina G. Maximum temperature and solar radiation as predictors of bipolar patient admission in an emergency psychiatric ward. Int J Environ Res Public Health. 2019;16(7):1140. pmid:30934957
                    • 84. Parker GB, Hadzi-Pavlovic D, Graham RK. Examining for any impact of climate change on the association between seasonality and hospitalization for mania. J Affect Disord. 2017;208:431–5. pmid:27846412
                    • 85. Triki T, Sellami R. Bipolar disorder and climatic factors. Psychiatry Psychol Disord. 2024;3(2).
                    • 86. Zhang R, Volkow ND. Seasonality of brain function: role in psychiatric disorders. Transl Psychiatry. 2023;13(1):65. pmid:36813773
                    • 87. Clery P, Hayes JF, Launders N, Thompson R, Kandola A, Osborn DPJ, et al. The association between outdoor ambient temperature and depression and mania: an ecological momentary assessment study. J Affect Disord. 2025;379:457–66. pmid:40081591
                    • 88. Brewerton TD, Putnam KT, Lewine RRJ, Risch SC. Seasonality of cerebrospinal fluid monoamine metabolite concentrations and their associations with meteorological variables in humans. J Psychiatr Res. 2018;99:76–82. pmid:29427844
                    • 89. Lewis KJS. Sleep disruption as a pathway to mania in bipolar disorder. 2017.
                      • 90. Vancampfort D, Stubbs B, Mitchell AJ, De Hert M, Wampers M, Ward PB, et al. Risk of metabolic syndrome and its components in people with schizophrenia and related psychotic disorders, bipolar disorder and major depressive disorder: a systematic review and meta-analysis. World Psychiatry. 2015;14(3):339–47. pmid:26407790
                      • 91. Mun S, Park K, Lee S. Evaluation of thermal sensitivity is of potential clinical utility for the predictive, preventive, and personalized approach advancing metabolic syndrome management. EPMA J. 2022;13(1):125–35. pmid:35265229
                      • 92. Cruz E, D’Alessio SJ, Stolzenberg L. The effect of maximum daily temperature on outdoor violence. Crime Delinq. 2020;69(6–7):1161–82.
                      • 93. Cohn EG. The prediction of police calls for service: The influence of weather and temporal variables on rape and domestic violence. J Environ Psychol. 1993;13(1):71–83.
                      • 94. Cook MR, Emick D, Foley C, Beatty A, McCormick C, Shapiro M. Daily temperature predicts assault and may allow more efficient policing. Am Surg. 2012;78(4):E194–5. pmid:22472368
                      • 95. Burke M, González F, Baylis P. Higher temperatures increase suicide rates in the United States and Mexico. https://doi.org/10.1038/s41558-018-0222-x
                        • 96. Bando DH, Teng CT, Volpe FM, de Masi E, Pereira LA, Braga AL. Suicide and meteorological factors in São Paulo, Brazil, 1996-2011: a time series analysis. Revista Brasileira de Psiquiatria. 2017;39(3):220–7.
                        • 97. Bär S, Bundo M, de Schrijver E, Müller TJ, Vicedo-Cabrera AM. Suicides and ambient temperature in Switzerland: a nationwide time-series analysis. Swiss Med Wkly. 2022;152:w30115. pmid:35262317
                        • 98. Yarza S, Vodonos A, Hassan L, Shalev H, Novack V, Novack L. Suicide behavior and meteorological characteristics in hot and arid climate. Environ Res. 2020;184:109314. pmid:32187563
                        • 99. Wang X, Lavigne E, Ouellette-kuntz H, Chen BE. Acute impacts of extreme temperature exposure on emergency room admissions related to mental and behavior disorders in Toronto, Canada. J Affect Disord. 2014;155:154–61. pmid:24332428
                        • 100. Mazlomi A, Golbabaei F, Farhang Dehghan S, Abbasinia M, Mahmoud Khani S, Ansari M, et al. The influence of occupational heat exposure on cognitive performance and blood level of stress hormones: a field study report. Int J Occup Saf Ergon. 2017;23(3):431–9. pmid:27852154
                        • 101. Romanello M, di Napoli C, Green C, Kennard H, Lampard P, Scamman D, et al. The 2023 report of the Lancet Countdown on health and climate change: the imperative for a health-centred response in a world facing irreversible harms. Lancet. 2023;402(10419):2346–94. pmid:37977174
                        • 102. Layton JB, Li W, Yuan J, Gilman JP, Horton DB, Setoguchi S. Heatwaves, medications, and heat-related hospitalization in older Medicare beneficiaries with chronic conditions. PLoS One. 2020;15(12):1–15.
                        • 103. Centers for Disease Control and Prevention (CDC). Heat and Medications – Guidance for Clinicians. 2025. [cited 2026 May 4]. https://www.cdc.gov/heat-health/hcp/clinical-guidance/heat-and-medications-guidance-for-clinicians.html#print
                          • 104. Mosadeghrad AM, Isfahani P, Eslambolchi L, Zahmatkesh M, Afshari M. Strategies to strengthen a climate-resilient health system: a scoping review. Global Health. 2023;19(1):62. pmid:37641052
                          • 105. Corvetto JF, Helou AY, Kriit HK, Federspiel A, Bunker A, Liyanage P, et al. Private vs. public emergency visits for mental health due to heat: an indirect socioeconomic assessment of heat vulnerability and healthcare access, in Curitiba, Brazil. Sci Total Environ. 2024;934:173312. pmid:38761938
                          • 106. Sera F, Hashizume M, Honda Y, Lavigne E, Schwartz J, Zanobetti A, et al. Air conditioning and heat-related mortality: a multi-country longitudinal study. Epidemiology. 2020;31(6):779–87. pmid:33003149
                          • 107. White MP, Elliott LR, Grellier J, Economou T, Bell S, Bratman GN, et al. Associations between green/blue spaces and mental health across 18 countries. Sci Rep. 2021;11(1):8903. pmid:33903601
                          • 108. Afzal F, Das A, Chatterjee S. Drawing the linkage between women’s reproductive health, climate change, natural disaster, and climate-driven migration: Focusing on low- and middle-income countries - a systematic overview. Indian J Commun Med. 2024;49(1):28–38.
                          • 109. Mason AE, Kasl P, Soltani S, Green A, Hartogensis W, Dilchert S, et al. Elevated body temperature is associated with depressive symptoms: results from the TemPredict Study. Sci Rep. 2024;14(1):1884. pmid:38316806
                          • 110. Alizadeh S, Bridge CE, Judd BH, Eapen V. Home indoor environmental quality and attention deficit hyperactivity disorder. Sustainability. 2023;15(4):2899.
                          • 111. Zinabu S, Gasmelseed H, Wheaton N, Girma F, Wong C, Tabraiz SA, et al. Stimulant medications effects in heat-related illness in ADHD patients: a large database study. Front Psychiatry. 2024;15:1509385. pmid:39758443
                          • 112. Corona JC. Role of oxidative stress and neuroinflammation in attention-deficit/hyperactivity disorder. Antioxidants (Basel). 2020;9(11):1039. pmid:33114154
                          • 113. Miller AH, Raison CL. The role of inflammation in depression: from evolutionary imperative to modern treatment target. Nat Rev Immunol. 2016;16(1):22–34. pmid:26711676