INTRODUCTION
Literature encompasses a multitude of interdiscipli-nary studies in biometeorology, clinical psychology, psychiatry, and related fields that investigate the influence of meteorological factors on human functioning at both the population and individual levels [1-4]. Recent analyses have also considered the broader context of the glo-bal climate crisis, highlighting its growing significance in health research [5, 6]. Climate change has been linked not only to social and economic disruptions but also to health risks, including those associated with air pollution, extreme heat, and weather anomalies [6]. These environmental stressors can have substantial psychological and somatic impacts on affected populations [1-3].
Evidence from various regions underscores the mental health consequences of extreme weather. In the UK, meta-analytic data associates floods, storms, and heatwaves with depression, anxiety, post-traumatic stress disorder (PTSD), and suicidal behavior [1]. Findings from the Asia-Pacific region link extreme weather with adverse outcomes, including increased rates of stress-related and affective symptoms [2]. A scoping review of African studies identified associations between droughts, floods, and heat exposure and a range of psychological problems while also highlighting significant gaps in longitudinal data and diagnostic verification [3]. Research from the Amazon region further suggests that local weather and biomass burning contribute to respiratory and systemic symptoms in children [4].
In addition to extreme events, meteoropathy and meteo-sensitivity have garnered increasing interest among researchers. These terms describe symptom patterns that encompass both somatic and psychological manifestations triggered by changes in weather conditions [9].
Meteoropathy is not recognized as a diagnostic or nosological entity in current classifications (DSM-5, ICD-10 and ICD-11) but refers to a recurrent set of symptoms associated with atmospheric variability, whereas meteo-sensitivity denotes an individual’s biological susceptibi-lity to such factors [9]. Symptoms included irritability, mood fluctuations, fatigue, sleep disturbances, and pain, suggesting a potential link between environmental stressors and psychopathological processes. However, despite these associations the underlying mechanisms remain unclear.
The concepts discussed above have only recently gained attention, partly explaining the limited amount of empirical data. In contrast, seasonal affective disorder (SAD) is well established in diagnostic classification and serves as an example of how environmental factors can modulate psychiatric symptoms. Moreover, research has increasingly explored climate-related affective responses, including anxiety and grief, in the context of environmental change [5, 6]. In parallel, studies indicate that extreme weather events can aggravate somatic conditions, with asthma exacerbations reported during episodes of heat, thunderstorms, and hurricanes – highlighting the interconnected nature of physical and psychological health risks [7]. Reviews of data from European studies further emphasize the health burden of extreme weather events while also noting the heterogeneity of findings and metho-dological constraints [8]. This review aimed to synthesize evidence on the impact of meteorological conditions on mental and somatic health, with a particular focus on meteoropathy, meteosensitivity, and their links to psychopathology. It also identifies current gaps in knowledge and underscores the need for further research using standardized diagnostic tools [9] and approaches that integrate psychological and environmental perspectives.
METHODS
Initially, 228 studies relevant to the objectives of this review were identified. Subsequently, publications were selected that comprised original studies, meta-analyses, theoretical papers and systematic reviews which provided evidence of the relationship between meteorological variability and physiological and psychological responses, as well as elucidating the biological mechanisms that may mediate this influence. Publications were identified through searches of the PubMed, Google Scholar, Scopus, and Web of Science databases, employing keywords pertinent to the subject matter of the review, such as “weather,” “HPA axis,” “meteoropathy,” “somatic symptoms,” “heat,” “psychoimmunology” and other terms describing the impact of weather conditions on health, as well as combinations of these. Only texts published between 2000 and 2025 were analyzed. Exclusion criteria included case studies, studies with poor methodology, studies whose purpose was not consistent with the purpose of this review, those in which variables were not adequately controlled, those in which the sample size was too small (fewer than 20 subjects), or those that did not provide substantial evidence on mechanisms related to meteorology. Of the 109 publications, 43 were included in the review, analyzed and described in this paper. Each text was critically reviewed for methodological quality, sample size, research tools used, and conclusions regarding the biological mechanisms relevant to the area under review.
METEOROPATHY AND METEOSENSITIVITY
Meteoropathy and meteosensitivity are complex phenomena in which meteorological factors, such as changes in atmospheric pressure, humidity, temperature, insolation, and the movement of weather fronts, provoke or exacerbate somatic and psychological symptoms in susceptible individuals [10, 11]. Recent reviews estimate that 20-30% of the general population is affected, with a higher prevalence observed among women, particularly during menopause, and older adults [9, 10, 12, 13]. Po- pulation-specific moderators further shape vulnerability to these conditions. In older adults, multimorbidity and age-related physiological changes complicate the dia-gnostic distinction between weather-related symptoms and coexisting medical conditions [12]. Psychiatric comorbidities, particularly affective disorders, can amplify symptom perception, whereas somatic conditions, such as cardiovascular disease, may increase the burden of meteoropathic complaints [9, 10]. These moderators illustrate that clinical manifestations of meteoropathy and meteosensitivity are heterogeneous and shaped by biological, demographic, and clinical characteristics rather than representing uniform responses across populations. In light of these differences, clear conceptual distinctions remain important. Meteosensitivity refers to a subjective perception of how weather influences mood, whereas meteoropathy denotes the presence of specific somatic or psychiatric symptoms [9]. The METEO-Q questionnaire has been proposed as a diagnostic tool for distinguishing between these conditions [9].
Among the symptoms associated with meteoropathy, the most prevalent are sleep disturbances (insomnia or excessive sleepiness), irritability, mood fluctuations, anxiety, depression, headaches, joint pain, palpitations, fatigue, gastrointestinal issues, and elevated blood pressure [10, 14]. Some reports describe additional neurological complaints, such as transient cognitive difficulties and problems with concentration, suggesting a broader spectrum of symptomatology [12].
From a neurobiological perspective, the impact of weather conditions on the functioning of the hypothalamic–pituitary–adrenal (HPA) axis is of paramount importance. It has been observed that variations in atmospheric pressure may lead to increased secretion of adrenocorticotropic hormone (ACTH) and cortisol, which can result in heightened anxiety symptoms, irritability, and somatic disorders [15]. Concurrently, endor-phins are reduced, which lowers the pain threshold and facilitates the occurrence of pain [16]. The possible involvement of serotonergic and noradrenergic pathways has been suggested in the context of mood regulation and stress reactivity, although these mechanisms remain hypo-thetical [12].
These mechanisms have been substantiated by experimental investigations using animal models. Sato et al. [17] demonstrated that a reduction in barometric pressure activates neurons within the vestibular nucleus and hypothalamus, as evidenced by an increased expression of c-Fos protein, a marker indicative of neuronal arousal. Similarly, Kurauchi et al. [16] observed heightened activity in the amygdala in such conditions, suggesting that limbic structures are involved in emotional processing. Reviews report that these findings are consistent with clinical observations of enhanced limbic reactivity to weather changes [12].
Weather exerts an influence on neurotransmitters associated with mood regulation, with serotonin playing a particularly significant role owing to its involvement in modulation of mood, regulation of circadian rhythm, and activity in the HPA axis. Disruptions in these functions can increase the susceptibility to somatization and meteo-rotropic reactions [18, 19]. Some studies have suggested a potential involvement of dopamine and norepinephrine in response to weather-induced stress [20].
Temperamental predisposition is also a critical factor, as individuals exhibiting cyclothymic, anxiety, and dysthymic traits are more likely to exhibit meteosensitivity and pronounced meteoropathic reactions [21]. A potential mediator of this relationship is a tendency towards rumination, characterized by a persistent focus on personal ailments and well-being, which can exacerbate the perception of symptoms [20]. Caspi et al. [22] demonstrated that genetic variation in the serotonin transporter gene moderates the impact of environmental stressors on the risk of developing affective disorders, highlighting the interaction between biological vulnerability and environmental conditions. This aligns with data indicating that individuals with high levels of neuroticism or elevated BIS (behavioral inhibition system) scores report an increased severity of meteoropathy, particularly in younger adults [23, 24].
Electromagnetic factors have been hypothesized as potential contributors to symptoms of meteoropathy, although the current evidence remains speculative [10, 12]. Liebell [25] further suggested that meteoropathic individuals might perceive weather changes due to electromagnetic influences, even in the absence of direct atmospheric indicators. While these mechanisms remain hypothetical, clinical observations consistently describe symptoms of meteoropathy as following a cyclical pattern that occurs immediately before or after weather changes. This condition is adversely affected by high humidity (> 70%) and heat (> 30°C), which can result in dehydration, electrolyte imbalances, and exacerbated physical symptoms [14]. Although some patients exhibit a degree of adaptation to weather conditions, many continue to experience persistent symptoms over time [9]. Recent reviews have described preventive measures, such as physi-cal activity, stress management, and appropriate supplementation with magnesium and vitamin B, as potentially helpful in reducing the severity of symptoms [10]. The use of biometeorological forecasts is also mentioned as a way of anticipating an exacerbation of symptoms and supporting preventive strategies [12].
SEASONAL AFFECTIVE DISORDER
Over the past four decades, SAD has been extensively documented and its mechanisms of onset are well understood. Although not recognized as a distinct diagnostic entity, it plays a significant role in the diagnosis and treatment of affective disorders. In diagnostic classifications such as the DSM-5, the seasonal pattern of depression is considered a specifier for episodes of unipolar or bipolar depression, denoted as “with seasonal pattern.” The criteria include the regular occurrence of depressive symptoms during specific times of the year, most commonly in fall or winter, remission in spring or summer, and the stability of this pattern for a minimum of two years. Similarly, ICD-11 does not classify SAD as a separate nosological entity, but it can be coded as a depressive episode with seasonal features.
Circadian and seasonal variations are important because they affect the regulation of mood, sleep patterns, and susceptibility to seasonal affective disorder. Alterations in photoperiod further modulate brain function, particularly influencing the activity of the pineal gland, where melatonin is secreted. Melatonin regulates circadian rhythms by activating two types of melatonin receptors, MT1 and MT2, and its activity can be inhibited by melanopsin [26, 27]. Research has demonstrated that individuals with SAD during winter exhibit selective attenuation of the cortisol awakening response (CAR), while maintaining the dynamics of all-day cortisol secretion. This indicates seasonal morning hyporeactivity of the HPA axis, which is absent in both healthy individuals and those with SAD during summer. Decreased CAR in winter correlates with heightened symptoms of depression, anxiety, stress, and low arousal, presenting a consistent picture of diminished mental functioning [28]. Neuroimaging studies have revealed seasonal differences in the activity of serotonergic 5-HT1A receptors and serotonin transporters, which are more active during months of increased sunlight exposure [29]. Furthermore, post-mortem studies have indicated reduced activity of tyrosine hydroxylase and dopamine transporters in midbrain neurons during winter, suggesting a seasonal decline in dopamine synthesis and reuptake [30].
There is a genetic component in the development of SAD that is potentially linked to circadian rhythm function. The most significant finding in the Genome-Wide Association Study (GWAS) pertains to the zinc finger and the BTB domain, which contains the 20 (ZBTB20) gene. It encodes a protein that regulates the expression of other genes and influences brain development and function. Individuals with SAD are more likely to possess a variant of this gene, which is associated with decreased activity in the temporal cortex. Notably, genes regulated by ZBTB20 were more frequently associated with SAD, supporting the hypothesis that it contributes to susceptibility to the disorder. These findings suggest that in certain individuals, sensitivity to seasonal mood changes may be attributed to genetically determined variations in the regulation of diurnal rhythms [31].
THE IMMUNOSEASONAL THEORY
The immunoseasonal theory of psychiatric disorders suggests that seasonal variations in relative humidity influence the balance of Th1-Th2 immune responses. In individuals with susceptibility to immunogenetic factors, this modulation can result in depressive, manic, or psychotic symptoms [32]. During autumn and winter increased humidity and a higher incidence of viral infections (e.g., RSV, influenza, and norovirus) stimulate the activation of the Th1 response. This activation leads to elevated levels of proinflammatory cytokines (IL-1β, IL-2, IL-6, TNF-α, IFN-γ, and sIL-2R) produced by Th1 lymphocytes, M1 monocytes, and microglia. These cytokines may penetrate the central nervous system via the leaky blood-brain barrier, active transport, or vagus nerve pathway, among other routes, thereby reducing the acti-vity of the prefrontal cortex and mesolimbic structures, which in turn leads to symptoms of depression [33, 34].
During the spring and summer months a decrease in the infectious load, coupled with an increase in allergic reactions, results in the compensatory dominance of Th2. Th2 lymphocytes, Treg, M2 macrophages, and astrocytes produce anti-inflammatory cytokines (IL-4, IL-5, IL-10, and IL-13) that limit the Th1 response. In individuals susceptible to psychotic or manic disorders, excessive activation of Th2 can stimulate glutamatergic and dopaminergic pathways within the cortex and limbic system, potentially leading to paranoid, delusional, or manic symptoms [35, 36]. In the context of bipolar affective disorder (BD), cytokine profiles vary by phase: IL-6 is predominant during depressive episodes; IL-4 is prevalent in the euthymic state; and IL-2, IL-4, and IL-6 are elevated during manic episodes. Furthermore, hyperintense white matter lesions, particularly in the frontal lobes, are frequently observed and occur up to 2.5-5.7 times more often than in the general population. These lesions may impede neuronal conduction and influence psychotic symptoms [37].
In schizophrenia, the Th2 phenotype is predominant and is accompanied by a diminished Th1 response. Chronic low-grade neuroinflammation is instrumental in the activation of microglia and the disruption of dopaminergic, glutamatergic, and other neurotransmitters, resulting in persistent cognitive deficits, which are also observed in healthy relatives of patients [36, 38]. Another mechanism involves activation of the HPA axis in response to stress, which, through hypercortisolemia and an increase in pro-inflammatory cytokines, heightens susceptibility to affective and psychotic disorders. Of particular significance is the Th17 pathway (IL-17, IL-6, TGF-β), which is associated with anxiety and oxidative stress [39].
Waszkiewicz also proposes the “flashback effect” hypo-thesis, suggesting that dormant viruses or toxins can be reactivated without re-exposure, potentially explaining the recurrence of psychopathological symptoms [40, 41].
This theory integrates immunological, meteorological, and genetic factors, thereby offering novel diagnostic and therapeutic possibilities for psychiatry. It may also partially elucidate phenomena such as meteoropathy, characterized by a decline in mental and physical well- being in response to changing weather conditions, parti-cularly humidity.
MEDICALLY UNEXPLAINED SYMPTOMS
Meteosensitive individuals or those exhibiting meteoropathy frequently report symptoms such as headaches, fatigue, insomnia, irritability, and gastrointestinal complaints. Similar symptoms have been observed in patients with medically unexplained symptoms (MUS). In many cases, these symptoms are not substantiated by diagnostic tests, nor do they meet the full diagnostic criteria for recognized diseases [42]. MUS is associated with a significant increase in the utilization of healthcare, reduced quality of life, and the risk of iatrogenic harm due to repeated diagnostic procedures [43].
Research indicates that MUS is characterized by a high severity of subjectively experienced symptoms without confirmation of their etiology through imaging or laboratory studies, as well as a significant functional burden on the patient [42, 44]. In older adults, diagnostic challenges are exacerbated by multimorbidity, which can obscure the differentiation between medically explained and unexplained symptoms, leading to an overestimation or underestimation of the severity of symptoms [43].
Meteoropathy and meteosensitivity may similarly be regarded as categories describing recurring patterns of symptoms that fall outside traditional disease entities but substantially affect individual well-being. Although the prevalence rates of somatoform disorders tend to be lower in later life, this may reflect difficulties in distinguishing MUS from comorbid conditions, rather than a true decrease in their incidence [45].
Cognitive processes, such as selective attention to bodily sensations and their interpretation as threats, are believed to play a significant role in the persistence of MUS, reinforcing beliefs about illness despite the lack of objective findings [46]. This phenomenon is closely related to the concept of somatosensory amplification, which describes the tendency to perceive normal bodily sensations as unusually intense and distressing [47]. These mechanisms are frequently accompanied by heightened rumination, anxiety, and catastrophizing. Previous experiences of illness and inconclusive medical examinations may further strengthen maladaptive health beliefs [48]. Environmental factors, including odour perception and environmental concerns, have also been reported to intensify symptom perception in other unexplained syndromes, suggesting the role of psychosocial mediators in symptom persistence [49].
From a neurobiological standpoint, the brain-centered model proposed by Baloh [47] synthesizes the findings related to physiological symptoms of stress sensory processing, and learning. This model posits that increased interoceptive attention and an atypical top-down modulation of sensory input can intensify normal bodily signals, resulting in persistent symptoms [47]. Activation of the HPA axis and heightened sympathetic activity related to stress may exacerbate the perception of symptoms, although evidence regarding these mechanisms remains inconsistent. Neural network plasticity, particularly within the limbic and somatosensory circuits, has also been implicated in the persistence of symptoms, suggesting that prior experiences and expectations may influence sensory processing over time [47]. These mechanisms are conceptualized as interacting networks rather than isolated pathways, and their precise contribution to MUS continues to be explored [50].
Although none of the reviewed sources explicitly classified meteoropathy or meteosensitivity as forms of MUS, the similarities observed in symptom patterns and features, such as heightened stress reactivity and absence of clear structural pathology, align with the mechanisms described in MUS research. These parallels remain theoretical and have not yet been directly confirmed [43, 47, 51]. Environmental research on unexplained syndromes similarly notes overlaps in conditions, such as multiple chemical sensitivity or sick building syndrome, where symptoms are triggered by environmental factors without an identifiable pathology [49]. These observations underscore the need for future longitudinal studies to better delineate the boundaries and mechanisms underlying these associations [43].
From a clinical perspective, the management of these symptoms may benefit from psychoeducation, the moni-toring of symptom-weather associations, and adaptive interventions aligned with seasonal patterns, particularly in vulnerable populations such as older adults [43]. Baloh [47] emphasized that effective care should transition from exhaustive diagnostic testing to interventions targeting the perception of symptoms and the regulation of stress, which is consistent with the biopsychosocial framework. This approach may also inform management strategies for meteoropathy [49].
CONCLUSIONS
The reviewed literature indicates that weather conditions may affect somatic and psychological symptoms through the interaction of biological, cognitive, and psychosocial factors. Meteoropathy and meteosensitivity are associated with complaints such as headaches, fatigue, instability of mood, anxiety, and sleep disturbances. These findings suggest that environmental factors interact with psychopathological processes, particularly among individuals with affective vulnerability. Cognitive-emotional mechanisms, including selective attention to bodily sensations, rumination, and catastrophic interpretation, contribute significantly to the persistence of symptoms.
The immunoseasonal theory of psychiatric disorders proposes that seasonal shifts in immune function influence mood and psychotic symptoms. This model links fluctuations in Th1/Th2 immune responses, cytokine concentrations, and microglial activation with the seasonality observed in disorders such as bipolar disorder and schizophrenia. Although these observations support the plausibility of the theory, they remain preliminary and require empirical validation [32].
The concept of somatosensory amplification, discussed in the context of MUS, provides a useful framework for understanding how neutral bodily sensations may be perceived as distressing [47]. This model aligns with the brain-centered approach to MUS, which emphasizes altered central processing rather than structural pathology [47]. Although meteoropathy shares some clinical features with MUS, current evidence does not support the classification of these conditions; any overlap remains a hypothesis that requires further research [43, 47]. Bio-logical factors have also been discussed in literature as potential mediators. Variability in the HPA axis, altera-tions in circadian rhythms, and changes in serotonergic and noradrenergic pathways have been described as possible contributors to weather-related symptoms, although the findings remain inconsistent [47]. These mechanisms are viewed as interacting networks rather than isolated causes of symptom expression.
From a diagnostic perspective weather-related symptoms pose challenges, particularly in older adults, where multimorbidity can obscure assessment and lead to a misinterpretation of the symptom burden [43]. Psychosocial mediators, including environmental concerns, may further intensify the perception and persistence of symptoms [49]. The clinical implications highlight the usefulness of the biopsychosocial model, which integrates psychopathological, somatic, and environmental factors. Psychoeducation, symptom monitoring in relation to the weather, and interventions targeting maladaptive beliefs about illness may enhance patient care without unnecessary medicalization [47, 49]. Future studies should employ longitudinal designs, use standardized diagnostic tools, and integrate psychopathological assessments with biological data to better define causal pathways. Such research is necessary to determine whether weather acts as a trigger, modulator, or background factor for mental and physical health. In conclusion, weather appears to function as a non-specific environmental stressor that can influence symptom expression through a combination of biological and psychological pathways. Current evidence supports a cautious interpretation of these associations and underscores the need for further investigation in order to refine diagnostic understanding and inform preventive and therapeutic strategies.
Future research should prioritize longitudinal, hypo-thesis-driven designs capable of testing causal pathways between meteorological factors and mental and physical health outcomes. Emphasis should be placed on translational objectives, including the development of standardized diagnostic measures and the assessment of tailored interventions. Such approaches would not only improve comparability across studies but also provide a stronger empirical basis for integrating weather-related health research into clinical practice.
This narrative review inherently lacks the methodo-logical rigor of systematic reviews. Although the selection of studies is extensive, it does not incorporate a formal risk-of-bias assessment, predefined timeframes, or exhaustive search strategies, potentially limiting the comprehensiveness of the findings. The literature analyzed here is heterogeneous in terms of study design, population, and diagnostic tools, which restricts direct comparability and synthesis. Furthermore, the possibility of publication bias cannot be excluded as the majority of available studies are observational and may overrepresent positive associations. The biological pathways discussed, including HPA axis dysregulation, modulation of the immune system, and alterations to the functioning of neurotransmitters, remain largely theoretical in the context of meteoropathy and meteosensitivity, with limited empirical confirmation. Certain sections, particularly those concerning vulnerable groups and coping strategies, are less developed than the discussion of seasonal affective disorders, reflecting both gaps in evidence and an imbalance in the current research focus. Moreover, while the clinical implications have been outlined, their practical applicability remains limited owing to the scarcity of interventional data. These limitations necessitate a cautious interpretation of the conclusions and underscore the need for longitudinal, standardized, and clinically oriented studies to strengthen the evidence base and support its translation into medical practice.
