Journal for Lipids in Health and Disease
1Department of Economic, Psychological and Communication Sciences, Niccolò Cusano University, 00191 Rome, Italy
2Department of Medical Sciences and Public Health, University of Cagliari, 09124 Cagliari, Italy
Cite this as
D’Aleo E, Scarparo T, Greco EA, Campedelli L, Cicoli A, Spagna S, et al. Intermittent Fasting, Interoceptive Awareness, and Emotional Regulation: A Psychobiological Narrative Review. J Lipids Health Dis. 2026;2(1):001-010. Available from: 10.17352/jlhd.000002
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© 2026 D’Aleo E, 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.Intermittent fasting (IF) has gained increasing attention as a metabolic intervention that can improve insulin sensitivity, lipid profiles, and systemic inflammatory markers. A central feature of IF is the shift toward lipid-based energy metabolism, characterized by enhanced lipolysis, mobilization of free fatty acids, and increased production of ketone bodies. These lipid-derived substrates not only sustain energy demands during fasting states but also function as bioactive signaling molecules involved in neuroendocrine regulation and cellular stress adaptation.
Despite the growing metabolic literature, the psychological and experiential dimensions of intermittent fasting (IF) remain comparatively underexplored. This narrative review advances a psychobiological framework in which IF is understood as a controlled metabolic stressor engaging lipid metabolism, stress physiology, and emotional regulation processes. Drawing on interdisciplinary evidence from neuroendocrinology, affective neuroscience, and clinical psychology, we examine how fasting-related metabolic transitions influence both peripheral and central systems.
Suppose modulates stress-related pathways, including hypothalamic–pituitary–adrenal (HPA) axis activity, autonomic balance, and ketone body signaling. Within this framework, lipid-derived signals—particularly free fatty acids and ketone bodies—may influence central nervous system functioning by modulating neuroinflammatory processes, mitochondrial efficiency, and stress-sensitive neural circuits involved in emotional processing. Central to this model is interoception, defined as the perception and integration of internal bodily signals. Interoceptive processing is here understood as a modulatory interface rather than a direct causal mechanism, shaped by metabolic signals, lipid availability, and individual neuroendocrine responsiveness.
Empirical and clinical observations suggest heterogeneous emotional outcomes during IF. While some individuals report improved emotional clarity and regulatory capacity, others experience increased irritability, cognitive rigidity, or anxiety. These divergent responses appear to be mediated by interoceptive sensitivity, psychological history, and trait-level vulnerabilities such as perfectionism, anxiety sensitivity, or emotional suppression. Particular attention is given to potential clinical risks in individuals with eating disorder histories, trauma exposure, or heightened somatic vigilance, underscoring the importance of psychological screening when IF is considered in applied contexts. These observations should not be interpreted as clinical recommendations, but rather as emerging psychobiological patterns arising from the interaction between lipid metabolism, stress physiology, and emotional regulation.
Current evidence is limited by a scarcity of longitudinal and integrative studies combining metabolic biomarkers with validated psychometric assessments. By integrating lipid metabolism with interoceptive and affective processes, future research adopting mixed-method designs may better clarify both the therapeutic potential and the psychological boundaries of intermittent fasting as a psychobiological intervention.
In recent years, intermittent fasting (IF) has attracted growing attention within both scientific communities and the public domain. Initially promoted for its potential to improve metabolic health through effects on insulin sensitivity, lipid metabolism, and systemic inflammation, IF has progressively expanded into broader health-related contexts, including aging, cancer prevention, and cognitive performance [1,2]. A defining metabolic feature of intermittent fasting is the shift from predominantly glucose-based energy utilization toward greater reliance on lipid substrates. This transition involves increased lipolysis, mobilization of circulating free fatty acids, and enhanced ketone body production. Beyond their role in sustaining energy demands during fasting, these lipid-derived substrates are increasingly recognized for their involvement in cellular stress responses and neuroendocrine signaling pathways. Accordingly, short overnight fasting intervals that do not induce a measurable shift toward lipid utilization are not the primary focus of the present framework.
Despite this proliferation of metabolic research, most studies have predominantly emphasized physiological and biochemical outcomes, often overlooking the subjective, experiential, and psychological dimensions of fasting. As a result, IF is rarely examined in terms of its psychobiological effects—that is, how metabolic shifts interact with internal bodily awareness, emotional processing, and individual psychological responses. Yet fasting does not act solely on biomarkers; it also alters how bodily states are perceived, how emotions are regulated, and how cognitive control is experienced. These changes are not merely epiphenomena of metabolism, but may meaningfully shape adherence, tolerability, and the overall impact of fasting practices.
From a psychobiological perspective, IF can be conceptualized as a controlled metabolic stressor that activates neuroendocrine pathways influencing both peripheral physiology and central nervous system functioning. This includes modulation of the hypothalamic–pituitary–adrenal (HPA) axis, alterations in autonomic balance, and increased production of ketone bodies, all of which intersect with affective and cognitive systems [3,4]. Within this framework, lipid-derived signals—particularly free fatty acids and ketone bodies—are increasingly recognized as bioactive mediators capable of influencing neuroinflammatory pathways, mitochondrial efficiency, and stress-responsive neural circuits.
In this context, the interoceptive system emerges as a potential interface linking metabolic changes to emotional and behavioral regulation. Interoception refers to the perception and integration of visceral and somatic signals related to hunger, satiety, fatigue, and arousal, and is mediated by a distributed neural network involving the insular cortex, anterior cingulate cortex, and brainstem nuclei [5,6]. Rather than functioning as a direct causal mechanism, interoceptive processing may modulate how metabolic and endocrine signals are subjectively interpreted and emotionally regulated.
Importantly, IF appears to amplify interoceptive signaling, which may result in divergent psychological outcomes. In some individuals, heightened interoceptive awareness may promote self-reflection and emotional clarity, whereas in others it may elicit hypervigilance, emotional instability, or dysregulation, particularly in the presence of pre-existing vulnerabilities [7,8]. These observations suggest that fasting-related metabolic transitions do not produce uniform psychological effects, but instead interact with individual differences in interoceptive sensitivity, stress responsivity, and emotion regulation strategies.
Accordingly, this narrative review proposes a psychobiological model in which IF is understood not simply as a nutritional intervention, but as an experiential metabolic event capable of shaping emotional tone and regulatory patterns through the interaction of lipid metabolism, neuroendocrine activity, and interoceptive processing. Rather than adopting a prescriptive or clinical stance, the aim is to integrate evidence from metabolic science, affective neuroscience, and clinical psychology to explore how and why emotional responses to fasting vary across individuals.
We begin by framing IF as a mild and potentially adaptive metabolic stressor, before examining its effects on interoceptive processes, emotional regulation, and psychological vulnerability. The overarching goal is to outline a theoretical model that accounts for both physiological benefits and potential psychological risks, while highlighting directions for future research that integrate metabolic markers with validated emotional and interoceptive measures.
This study follows the structure of a narrative review, designed to synthesize emerging evidence across metabolic science, affective neuroscience, and clinical psychology in relation to intermittent fasting (IF). In line with the exploratory and integrative aims of the manuscript, the review does not seek to provide a systematic meta-analysis of fasting outcomes, but rather to identify conceptual links and potential psychobiological mechanisms through which IF may influence emotional regulation and subjective experience. Particular attention was given to studies addressing lipid metabolism, neuroendocrine adaptation, and interoceptive processing within fasting contexts.
This narrative review focused primarily on human studies examining intermittent fasting (IF) in relation to metabolic, interoceptive, and emotional regulation processes. Eligible publications included original research articles and narrative or systematic reviews published in peer-reviewed journals between 2000 and 2024. Studies were considered for inclusion if they addressed at least one of the following domains: (1) metabolic and hormonal effects of IF, including lipid-related pathways; (2) interoceptive processing and bodily signal integration; or (3) psychological outcomes such as mood, affect regulation, and vulnerability traits associated with fasting.
Case reports, non-peer-reviewed literature, anecdotal or motivational content, and studies lacking clear methodological descriptions were excluded. Articles focusing exclusively on weight loss outcomes without reference to psychophysiological or regulatory mechanisms were not considered. Only studies published in English were included.
A non-systematic but structured literature search was conducted between July and December 2025 using the electronic databases PubMed, Scopus, and Google Scholar. Google Scholar was included to capture interdisciplinary and conceptual contributions not always indexed within biomedical databases. The search strategy combined terms related to intermittent fasting, metabolism, interoception, and emotional regulation, including:
Searches were restricted to peer-reviewed articles published in English. Preference was given to publications from the last 15 years (2010–2025), while seminal theoretical and empirical contributions in interoception and stress physiology published before this period were also considered when relevant [5]. Clinical studies, experimental investigations, theoretical models, and neuroimaging research were all eligible for inclusion. Given the narrative and conceptual nature of the review, no PRISMA flow diagram was applied.
Studies and reviews were included if they met one or more of the following criteria:
Animal studies were included only when they provided mechanistic insights directly relevant to psychobiological processes discussed in human fasting research, such as HPA axis modulation or stress adaptation.
Articles were excluded if they:
Included articles were grouped thematically and synthesized qualitatively. The analysis focused on identifying convergent patterns and conceptual links across disciplines rather than quantifying effect sizes. The primary thematic domains that emerged included: (1) intermittent fasting as a mild metabolic stressor and its neuroendocrine and lipid-related adaptations; (2) interoception as a modulatory interface between bodily states and emotional regulation; (3) individual variability in psychological and affective responses to fasting; (4) clinical risk profiles and contraindications; and (5) methodological limitations and gaps within the existing literature.
This thematic synthesis informed the organization and structure of the subsequent sections of the review.
Within a hormetic framework, intermittent fasting can be conceptualized as a mild and time-limited metabolic challenge capable of inducing adaptive cellular responses, particularly at the mitochondrial level. From this perspective, IF represents a form of mitohormetic stress, whereby transient energy deprivation promotes metabolic flexibility, redox balance, and cellular resilience rather than pathological stress activation.
Intermittent fasting (IF) can be conceptualized as a form of mild and potentially adaptive metabolic stress that induces coordinated neuroendocrine and cellular responses aimed at enhancing physiological resilience. During fasting periods, the organism undergoes a metabolic transition from glucose-based to lipid-based energy utilization, characterized by increased lipolysis, mobilization of circulating free fatty acids, and augmented ketone body production, alongside reduced insulin secretion and dynamic modulation of cortisol levels [1,9].
From a stress physiology perspective, IF is associated with a controlled activation of the hypothalamic–pituitary–adrenal (HPA) axis, resulting in transient elevation of cortisol plasma levels that appear to support metabolic adaptation rather than reflecting maladaptive or chronic stress activation [4,3]. This pattern aligns with the biological principle of hormesis, whereby exposure to moderate and time-limited stressors promotes adaptive capacity and improves tolerance to subsequent challenges [10]. Within this framework, lipid mobilization and ketone availability can be viewed as integral components of the organism’s adaptive response to metabolic stress.
Cortisol plays a pivotal regulatory role in the fasting response. While sustained hypercortisolemia is associated with metabolic dysfunction and affective disorders, short-term increases in cortisol levels during fasting may facilitate gluconeogenesis, enhance lipid mobilization, and support the metabolic switch toward ketone utilization—key features of adaptive fasting states [1,11]. Importantly, the magnitude and subjective impact of these endocrine responses appear to vary according to circadian timing, biological sex, and individual differences in stress reactivity [12].
Concomitantly, insulin levels decline markedly during fasting, leading to reduced anabolic signaling and enhanced lipolysis and ketogenesis. These metabolic shifts are tightly coupled with central signaling pathways, including modulation of oxidative stress and alterations in brain-derived neurotrophic factor (BDNF) expression [13]. Available evidence suggests that intermittent fasting is generally associated with an upregulation of brain-derived neurotrophic factor (BDNF), particularly during early and adaptive phases of metabolic switching. BDNF modulation appears to be time-dependent and context-sensitive, with potential attenuation or reversal under conditions of prolonged fasting, psychological stress, or reduced metabolic resilience. BDNF has been implicated in both metabolic plasticity and affective regulation, suggesting a possible mechanistic interface through which lipid-driven metabolic changes may influence cognitive and emotional processes.
Beyond their role as alternative energy substrates, ketone bodies—particularly β-hydroxybutyrate—function as signaling molecules capable of modulating histone deacetylase activity, inflammatory pathways, and synaptic function [14]. Through these mechanisms, ketone signaling may contribute to changes in neuronal efficiency and network stability that have been associated with reports of enhanced cognitive clarity and emotional regulation during fasting. Nevertheless, such effects are not uniform and appear to be modulated by substantial interindividual variability.
Finally, the capacity to tolerate fasting-induced metabolic stress appears to be associated with broader indices of physiological resilience, defined as the ability to maintain or rapidly restore homeostasis under challenge. IF has been linked to improvements in mitochondrial efficiency, activation of autophagic processes, and reductions in oxidative stress markers, all of which may contribute to a more robust and flexible stress-response system [15].
Taken together, these lipid-centered metabolic and neuroendocrine adaptations provide a biological foundation for understanding how IF may influence higher-order processes such as interoception and emotional regulation. At the same time, they raise important questions regarding individual susceptibility, particularly in populations characterized by altered stress-axis responsivity, metabolic inflexibility, or heightened sensitivity to internal bodily signals.
Intermittent fasting (IF) induces a complex cascade of endocrine adaptations that extend beyond metabolic regulation and contribute meaningfully to subjective experience and emotional functioning. From an integrative psychobiological perspective, hormonal responses to fasting do not merely reflect physiological adjustment to energy deprivation, but participate in shaping how internal bodily states are perceived, interpreted, and emotionally regulated over time.
One of the central endocrine pathways engaged during fasting involves the hypothalamic–pituitary–adrenal (HPA) axis. Short-term fasting has been associated with moderate increases in cortisol secretion, particularly during the early phases of metabolic switching [3,4]. While chronic HPA axis hyperactivation is well established as a risk factor for mood and anxiety disorders, transient cortisol plasma level elevations during fasting appear to support adaptive energy mobilization and metabolic flexibility [11]. At the same time, cortisol functions as a psychobiological signal of challenge, influencing vigilance, emotional tone, and stress appraisal. Individuals characterized by heightened stress sensitivity or altered HPA axis responsivity may therefore experience fasting-related endocrine changes not as adaptive, but as internally destabilizing.
Insulin and leptin modifications further contribute to the psychological salience of fasting-induced metabolic states. The reduction of circulating insulin during fasting facilitates lipolysis and ketogenesis, while also modifying central signaling pathways involved in satiety, reward processing, and emotional stability [9]. Leptin, traditionally viewed as a regulator of appetite and energy balance, also plays a role in affective modulation and motivational states. Decreased leptin signaling has been associated with irritability, emotional lability, and heightened stress sensitivity in psychologically vulnerable individuals [16]. Together, these findings suggest that lipid-driven metabolic shifts may intersect with emotional regulation systems through endocrine pathways encoding both energy availability and perceived safety.
A growing body of evidence highlights ghrelin as a particularly relevant hormone at the interface between metabolism and emotion. Ghrelin levels increase during fasting and have been shown to influence not only hunger perception but also anxiety-related behaviors, stress resilience, and reward sensitivity [17,4]. Experimental findings suggest that ghrelin may exert context-dependent and sometimes paradoxical effects, enhancing stress coping in certain conditions while amplifying anxiety and emotional reactivity in others. This dual role underscores how endocrine signals acquire psychological meaning through the interaction with individual history, trait vulnerability, and regulatory capacity.
Ketone bodies—particularly β-hydroxybutyrate—represent another key endocrine–metabolic signal with potential relevance for emotional and cognitive functioning. Beyond serving as alternative energy substrates, ketones act as signaling molecules capable of influencing neuroinflammatory processes, oxidative stress regulation, and synaptic plasticity [14]. Emerging evidence suggests that ketone-mediated pathways may support cognitive efficiency and mood stability, possibly through modulation of brain-derived neurotrophic factor (BDNF) expression and mitochondrial function [34], particularly during adaptive fasting phases, while remaining sensitive to individual vulnerability and duration of exposure.
However, these effects appear highly variable and may be attenuated or reversed in individuals with pre-existing affective instability or maladaptive interoceptive processing.
From a psychological standpoint, endocrine responses to fasting are inseparable from interoceptive processing. Hormonal fluctuations alter visceral sensations such as hunger, tension, fatigue, and arousal, which are subsequently interpreted through interoceptive networks involving the insular cortex and anterior cingulate cortex [6,7]. In individuals with high interoceptive awareness and flexible emotion regulation strategies, these bodily signals may be integrated without significant distress, fostering emotional clarity and adaptive self-regulation. Conversely, in individuals prone to somatic hypervigilance, anxiety sensitivity, or trauma-related dysregulation, the same endocrine signals may amplify emotional instability and reinforce maladaptive control strategies.
Taken together, these observations suggest that IF can be conceptualized as a psychobiological “stress test” that reveals the quality of mind–body integration rather than uniformly enhancing psychological well-being. Endocrine adaptations interact dynamically with lipid metabolism, psychological traits, emotional history, and regulatory patterns, giving rise to divergent subjective outcomes that cannot be reliably predicted by metabolic markers alone. Consequently, endocrine changes commonly described as metabolically beneficial do not necessarily translate into positive emotional effects across individuals.
For this reason, an interdisciplinary perspective is essential when IF is considered in clinical or preventive contexts. Endocrinological evaluation may benefit from being complemented by psychological screening focused on stress reactivity, emotion regulation strategies, interoceptive confidence, and current or past eating-related psychopathology. Without such integration, there is a risk of interpreting psychobiological distress as a transient adaptation phase, potentially overlooking early signs of emotional dysregulation.
In summary, endocrine responses to intermittent fasting play a pivotal role in shaping subjective experience and emotional regulation. Conceptualizing IF at the intersection of hormonal signaling, lipid metabolism, and psychological meaning allows for a more nuanced and ethically responsible interpretation of its potential benefits and limitations, particularly in populations characterized by latent vulnerability.
The concept of interoception—the perception and integration of internal bodily signals—has emerged as a central construct in affective neuroscience and psychophysiology [5,7]. Interoceptive processes allow individuals to detect changes in hunger, thirst, fatigue, visceral tension, and autonomic arousal, thereby contributing to self-regulation, emotional awareness, and the subjective sense of bodily identity. Rather than operating in isolation, interoception reflects the continuous integration of metabolic, autonomic, and endocrine signals into conscious and preconscious experience.
From a neuroanatomical perspective, interoception is supported by a distributed network involving the posterior and anterior insular cortices, anterior cingulate cortex, brainstem nuclei, and somatosensory pathways [6,18]. Within this network, the insula plays a pivotal role in mapping visceral and metabolic inputs and generating a subjective representation of internal states. This integrative process supports homeostatic regulation and informs behavior, mood, and cognitive appraisal, particularly under conditions of physiological change.
In the context of intermittent fasting (IF), interoceptive signaling appears to be modulated and, in many cases, amplified, especially during prolonged fasting windows. Fluctuations in hunger, energy availability, autonomic tone, and metabolic substrates become more salient, potentially enhancing bodily awareness while simultaneously increasing regulatory demands. Preliminary evidence suggests that fasting may increase interoceptive accuracy—the capacity to detect and interpret internal signals—although current findings remain limited and context-dependent [19].
A critical distinction must be drawn between interoceptive awareness and somatic hypervigilance. Interoceptive awareness refers to a mindful, non-judgmental engagement with internal bodily states and has been associated with adaptive emotional regulation and psychological flexibility. In contrast, somatic hypervigilance is characterized by heightened, anxiety-driven monitoring of bodily sensations and has been linked to anxiety disorders, panic symptoms, and functional somatic complaints [20,21]. This distinction is particularly relevant in fasting contexts, where physiological signals are inherently intensified.
Accordingly, IF may promote emotional clarity and regulatory stability in individuals with a high capacity for interoceptive modulation, while exacerbating dysregulation in those prone to catastrophic interpretations of bodily change. For example, fasting-related increases in heart rate, fatigue, or visceral tension may be experienced as manageable signals of metabolic adaptation in some individuals, but perceived as threatening or destabilizing in those with low interoceptive confidence or elevated anxiety sensitivity.
Interoceptive processing is also closely intertwined with the autonomic nervous system (ANS) regulation. Fasting-induced metabolic changes influence the balance between parasympathetic and sympathetic activity, with downstream effects on arousal, emotional tone, and stress responsiveness [22]. Reduced vagal tone, in particular, has been associated with diminished emotion regulation capacity and impaired somatic calming, potentially amplifying the emotional impact of intensified interoceptive signals.
Taken together, these observations suggest that interoceptive pathways may function as a modulatory interface between metabolic adaptations and emotional responses to IF, rather than as a direct causal mechanism. The psychological effects of fasting appear to depend less on metabolic changes per se than on how such changes are perceived, interpreted, and regulated at the interoceptive level. From this perspective, interoceptive sensitivity and regulation may represent key factors in differentiating adaptive from maladaptive emotional responses to fasting.
Enhancing interoceptive literacy—through psychoeducation, clinical monitoring, or body-oriented interventions—may therefore be relevant in identifying individuals for whom IF is well tolerated versus those at increased risk of psychological dysregulation. However, such considerations should be viewed as conceptual implications rather than clinical prescriptions, underscoring the need for integrative research designs that jointly assess metabolic, autonomic, and interoceptive variables.
While intermittent fasting (IF) has been associated with a range of physiological benefits, its effects on emotional regulation appear highly heterogeneous across individuals. Empirical findings and clinical observations suggest that fasting may modulate emotional tone in divergent ways, enhancing affective clarity and stability in some individuals while eliciting irritability, cognitive rigidity, or emotional distress in others, depending on psychological traits, regulatory capacity, and prior emotional history [23,24].
In a subset of individuals, IF has been associated with improved emotional clarity and reduced affective reactivity, potentially mediated by heightened interoceptive awareness and greater tolerance of internal bodily signals. These responses have been linked to improvements in mood, perceived self-regulation, and a sense of agency over impulses [25,26]. In such contexts, fasting may coincide with more effective top-down modulation of emotional responses, allowing for greater reflective capacity and reduced impulsivity.
Conversely, in individuals characterized by elevated trait anxiety, rigid perfectionism, or a history of affective dysregulation, IF may function as a psychological stressor rather than a regulatory aid. Several reports associate fasting with increased irritability, obsessive control, and emotional volatility, particularly during early adaptation phases or when fasting protocols are implemented in a rigid or inflexible manner [27,28]. In these cases, physiological changes inherent to fasting—such as hunger, fatigue, or autonomic arousal—may be interpreted as threatening or destabilizing, thereby undermining emotional stability.
A growing body of evidence suggests that stable psychological traits play a moderating role in these differential outcomes. High levels of anxiety sensitivity, perfectionism, need for control, and cognitive rigidity have been associated with greater emotional dysregulation during fasting [8,29]. In contrast, emotional benefits appear more likely in individuals with higher interoceptive confidence, flexible emotion regulation strategies, and prior familiarity with body-oriented practices such as mindfulness or contemplative disciplines.
Developmental and clinical history further shape emotional responses to fasting. Individuals with unresolved trauma, disordered eating patterns, or chronic affective instability may experience fasting as either a form of self-punishment or a means of achieving illusory control, potentially reinforcing maladaptive emotional and behavioral strategies [30,33]. These observations underscore how emotional outcomes associated with IF cannot be meaningfully interpreted in isolation from the broader psychological context.
Importantly, emotional responses to fasting are not static and may fluctuate across time and situational contexts. Environmental stressors, social support, cultural narratives surrounding fasting (e.g., moralization of hunger or valorization of self-denial), and individual expectations all contribute to how metabolic changes are emotionally experienced. This variability highlights the limitations of universal claims regarding the emotional effects of IF and reinforces the need for individualized, context-sensitive interpretation.
To facilitate conceptual clarity, a schematic overview of psychological profiles associated with differential emotional responses to fasting is presented in Table 1. This framework is intended as a descriptive synthesis of patterns emerging from the literature rather than as a clinical decision-making tool.
Although intermittent fasting (IF) is generally reported as well tolerated in metabolically healthy individuals, its application in clinical or psychologically vulnerable populations warrants careful and individualized consideration. Available evidence suggests that certain groups may be more susceptible to emotional dysregulation, somatic distress, or behavioral destabilization during fasting practices, particularly when fasting is implemented without adequate contextual or psychological support [27,30].
Individuals with a current or past diagnosis of eating disorders (EDs)—including anorexia nervosa, bulimia nervosa, and atypical restrictive presentations—appear to represent a particularly high-risk group. In these populations, fasting-related practices may inadvertently reinforce maladaptive patterns such as cognitive rigidity, compulsive control over bodily states, and emotional suppression, thereby increasing the risk of symptom exacerbation or relapse [30,31]. These risks highlight the importance of distinguishing between metabolically driven fasting protocols and fasting behaviors that may overlap with disordered eating dynamics.
Similarly, individuals with anxiety disorders—including generalized anxiety disorder, panic disorder, and health anxiety—may exhibit heightened physiological and emotional reactivity to fasting-induced bodily changes. Reductions in caloric intake and associated interoceptive shifts, such as hunger sensations, palpitations, or dizziness, may be misinterpreted as signals of threat or loss of control, fostering somatic hypervigilance and emotional destabilization [21,20]. In such cases, the psychological meaning attributed to bodily sensations may be more clinically relevant than the metabolic changes themselves.
Fasting may also pose specific challenges for individuals with a history of complex trauma, particularly when bodily control or restriction has previously served as a coping strategy or a perceived source of safety. Under these conditions, food restriction may activate dissociative responses, intrusive somatic memories, or shame-related affective states, potentially interfering with emotional regulation and ongoing therapeutic processes [32,33].
Importantly, many of the potential risks associated with IF are not purely metabolic in nature, but psychobiological, emerging from the interaction between fasting-induced physiological changes and pre-existing vulnerabilities in emotion regulation, stress responsivity, and interoceptive processing. From this perspective, IF should not be viewed as a universally neutral or inherently beneficial intervention, but rather as a context-dependent practice whose psychological impact varies according to individual regulatory capacity and clinical history.
Given these considerations, a preliminary psychological evaluation may be warranted when IF is considered in applied, preventive, or clinical contexts. Such evaluation may include assessment of eating-related attitudes, anxiety sensitivity, trauma history, and habitual emotion regulation strategies. For individuals identified as higher risk, alternative approaches that promote metabolic flexibility and bodily awareness—such as mindful eating, paced breathing techniques, or structured physical activity—may represent safer and more appropriate entry points.
When IF is implemented in clinical or integrative health settings, an interdisciplinary framework may be beneficial. Collaboration among medical professionals, psychologists, and nutrition specialists can facilitate monitoring of emotional well-being, somatic symptoms, and behavioral rigidity, particularly during early phases of fasting adaptation.
In summary, intermittent fasting is not intrinsically contraindicated in clinical populations; however, its safe and ethical application requires individualized evaluation, clear conceptual boundaries, and appropriate psychological oversight. Recognizing the psychobiological context in which fasting occurs is essential to minimizing risk and avoiding unintended psychological harm.
This narrative review examined intermittent fasting (IF) as a psychobiological phenomenon rather than a purely nutritional intervention. By integrating evidence from metabolic science, affective neuroscience, and clinical psychology, we proposed that IF may function as a controlled metabolic stressor whose effects on emotional regulation emerge from the interaction between lipid metabolism, neuroendocrine activity, and interoceptive processing.
Several key considerations emerge from this synthesis. First, IF is associated with neuroendocrine adaptations—including modest activation of the hypothalamic–pituitary–adrenal (HPA) axis, and changes in cortisol and insulin dynamics—that appear to support metabolic flexibility and adaptive stress responses [3,34]. These physiological changes are closely intertwined with lipid-based metabolic transitions, including enhanced lipolysis and ketone body signaling, which may influence central nervous system functioning. Importantly, such metabolic and endocrine signals also alter internal bodily states that are subjectively perceived and processed through interoceptive pathways involving the insular cortex and anterior cingulate cortex [5,6].
Second, the present review highlights how psychological outcomes associated with IF are strongly modulated by individual differences in interoceptive awareness, emotion regulation strategies, and trait-level vulnerabilities. While some individuals report improvements in emotional clarity and regulatory capacity, others—particularly those with heightened anxiety, trauma exposure, or perfectionistic tendencies—may experience affective destabilization or increased behavioral rigidity [24,8]. These findings are consistent with a differential susceptibility framework, suggesting that the psychological impact of fasting depends less on metabolic changes per se and more on how such changes are subjectively interpreted and regulated.
At the same time, the existing literature is characterized by several important limitations. Most IF studies prioritize metabolic and physiological endpoints, with limited incorporation of validated psychometric instruments assessing interoception, emotional regulation, or psychological vulnerability [26]. Moreover, the predominance of short-term interventions limits the ability to detect delayed, cumulative, or non-linear psychological effects [35]. This is particularly relevant given that early fasting phases may be accompanied by transient positive experiences—such as heightened clarity or energy—that may later evolve into emotional rigidity or blunted affect in susceptible individuals.
A further limitation concerns the lack of methodological integration across disciplines. Many studies assess metabolic biomarkers without parallel psychological evaluation, or conversely, examine mood-related outcomes without concurrent measurement of endocrine or metabolic variables. As a result, the mechanistic pathways linking lipid metabolism, neuroendocrine signaling, interoceptive processing, and emotional regulation remain insufficiently specified. Without integrated designs, it is difficult to determine whether observed emotional effects are primarily driven by hormonal changes, cognitive appraisal processes, or interoceptive modulation.
To advance the field, future research would benefit from mixed-method approaches that combine biological markers—such as cortisol, ketone bodies, lipid-related indices, and autonomic measures—with psychometrically robust assessments of interoception, emotion regulation strategies, and trait vulnerability [7]. Longitudinal designs are particularly needed to map temporal trajectories, distinguish between acute and sustained effects, and identify early indicators of maladaptive responses. Subgroup analyses may further clarify which individuals are more likely to benefit from IF and which may be at increased psychological risk.
Ethical considerations are also central to the interpretation and application of these findings. When IF is considered in clinical, preventive, or integrative health contexts, psychological screening, clear conceptual boundaries, and interdisciplinary supervision become essential. Without such safeguards, fasting practices—despite their metabolic rationale—may inadvertently reinforce maladaptive coping strategies or exacerbate underlying psychological vulnerabilities, particularly in at-risk populations.
Taken together, the findings synthesized in this review support a view of intermittent fasting as a context-dependent psychobiological intervention whose effects on emotional regulation are shaped by the dynamic interaction between metabolic signals, interoceptive processing, and individual psychological characteristics. As illustrated in Figure 1, IF may initiate a multilevel cascade beginning with lipid-driven metabolic and endocrine changes, followed by interoceptive integration, and culminating in either adaptive or maladaptive emotional outcomes depending on regulatory capacity and vulnerability. Within this framework, IF holds potential as a modulator of emotional functioning, but its application must remain selective, individualized, and grounded in both metabolic and psychological science.
Intermittent fasting (IF) represents a complex convergence of metabolic and psychological processes whose effects extend beyond traditional metabolic endpoints. As highlighted in this review, fasting-related adaptations involve not only insulin sensitivity and lipid metabolism but also neuroendocrine signaling, interoceptive processing, and emotional regulation pathways that remain insufficiently explored within current research frameworks. Conceptualizing IF as a psychobiological phenomenon, rather than solely as a nutritional strategy, allows for a more integrated understanding of its impact on subjective experience and emotional functioning.
The available evidence suggests that IF may operate as a controlled metabolic stressor, capable of interacting with interoceptive and affective systems in ways that, under certain conditions, coincide with improved emotional clarity or regulatory capacity. However, such outcomes are neither uniform nor predictable. Individual psychological characteristics—including anxiety sensitivity, perfectionistic traits, and trauma history—appear to shape vulnerability to emotional dysregulation, somatic hypervigilance, or rigid behavioral patterns during fasting. These findings underscore that the psychological effects of IF cannot be dissociated from individual regulatory capacity and contextual factors.
At present, the literature is limited by a lack of methodological integration between metabolic, endocrine, and psychological domains. Longitudinal and mixed-method research designs incorporating both physiological biomarkers and validated psychometric measures are needed to clarify temporal dynamics, identify differential response profiles, and specify the mechanisms through which fasting-related metabolic signals influence emotional regulation. Such approaches may help distinguish adaptive from maladaptive psychobiological responses and refine the interpretative boundaries of IF-based interventions.
Until more integrative evidence becomes available, IF should be approached with contextual awareness and individualized consideration, particularly in populations characterized by psychological vulnerability. Rather than being framed as a universally beneficial practice, intermittent fasting may be more appropriately understood as a selective, context-dependent intervention whose psychological impact emerges from the dynamic interaction between metabolic signals, interoceptive processing, and affective regulation capacity.
Conceptualization: Ettore D’Aleo, Mara Lastretti;
Methodology: Ettore D’Aleo, Tiziano Scarparo;
Formal Analysis: Lorenzo Campedelli, Andrea Cicoli;
Investigation: Lorenzo Campedelli, Emanuela A. Greco, Sabina Spagna;
Writing – Original Draft Preparation: Ettore D’Aleo, Tiziano Scarparo;
Writing – Review and Editing: Mara Lastretti, Ettore D’Aleo, Gavino Faa;
Supervision: Ettore D’Aleo, Mara Lastretti;
Project Administration: Ettore D’Aleo, Mara Lastretti.
All authors have read and agreed to the published version of the manuscript.
No generative artificial intelligence tools were used in the conception, writing, or interpretation of this manuscript.

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