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Explores the behavioral neuroscience of social attachment and its significance in establishing and maintaining human well-being.

Oxytocin has been revealed to work for anxiety suppression and anti-stress as well as for psychosocial behavior and reproductive functions. Oxytocin neurons are activated by various stressful stimuli. The oxytocin receptor is widely distributed within the brain, and oxytocin that is released or diffused affects behavioral and neuroendocrine stress responses. On the other hand, there has been an increasing number of reports on the role of oxytocin in allostasis and resilience. It has been shown that oxytocin maintains homeostasis, shifts the set point for adaptation to a changing environment (allostasis) and contributes to recovery from the shifted set point by inducing active coping responses to stressful stimuli (resilience). Recent studies have suggested that oxytocin is also involved in stress-related disorders, and it has been shown in clinical trials that oxytocin provides therapeutic benefits for patients diagnosed with stress-related disorders. This review includes the latest information on the role of oxytocin in stress responses and adaptation.

The development of alcohol use disorder (AUD) involves binge or heavy drinking to high levels of intoxication that leads to compulsive intake, the loss of control in limiting intake, and a negative emotional state when alcohol is removed. This cascade of events occurs over an extended period within a three-stage cycle: binge/intoxication, withdrawal/negative affect, and preoccupation/anticipation. These three heuristic stages map onto the dysregulation of functional domains of incentive salience/habits, negative emotional states, and executive function, mediated by the basal ganglia, extended amygdala, and frontal cortex, respectively. Sleep disturbances, alterations of sleep architecture, and the development of insomnia are ubiquitous in AUD and also map onto the three stages of the addiction cycle. During the binge/intoxication stage, alcohol intoxication leads to a faster sleep onset, but sleep quality is poor relative to nights when no alcohol is consumed. The reduction of sleep onset latency and increase in wakefulness later in the night may be related to the acute effects of alcohol on GABAergic systems that are associated with sleep regulation and the effects on brain incentive salience systems, such as dopamine. During the withdrawal/negative affect stage, there is a decrease in slow-wave sleep and some limited recovery in REM sleep when individuals with AUD stop drinking. Limited recovery of sleep disturbances is seen in AUD within the first 30 days of abstinence. The effects of withdrawal on sleep may be related to the loss of alcohol as a positive allosteric modulator of GABAA receptors, a decrease in dopamine function, and the overactivation of stress neuromodulators, including hypocretin/orexin, norepinephrine, corticotropin-releasing factor, and cytokines. During the preoccupation/anticipation stage, individuals with AUD who are abstinent long-term present persistent sleep disturbances, including a longer latency to fall asleep, more time awake during the night, a decrease in slow-wave sleep, decreases in delta electroencephalogram power and evoked delta activity, and an increase in REM sleep. Glutamatergic system dysregulation that is observed in AUD is a likely substrate for some of these persistent sleep disturbances. Sleep pathology contributes to AUD pathology, and vice versa, possibly as a feed-forward drive to an unrecognized allostatic load that drives the addiction process.

Stress is a state of the mind, involving both brain and body as well as their interactions; it differs among individuals and reflects not only major life events but also the conflicts and pressures of daily life that alter physiological systems to produce a chronic stress burden that, in turn, is a factor in the expression of disease. This burden reflects the impact of not only life experiences but also genetic variations and individual health behaviors such as diet, physical activity, sleep, and substance abuse; it also reflects stable epigenetic modifications in development that set lifelong patterns of physiological reactivity and behavior through biological embedding of early environments interacting with cumulative change from experiences over the lifespan. Hormones associated with the chronic stress burden protect the body in the short run and promote adaptation (allostasis), but in the long run, the burden of chronic stress causes changes in the brain and body that can lead to disease (allostatic load and overload). Brain circuits are plastic and remodeled by stress to change the balance between anxiety, mood control, memory, and decision making. Such changes may have adaptive value in particular contexts, but their persistence and lack of reversibility can be maladaptive. However, the capacity of brain plasticity to effects of stressful experiences in adult life has only begun to be explored along with the efficacy of top-down strategies for helping the brain change itself, sometimes aided by pharmaceutical agents and other treatments.

Introduction: Allostatic load refers to the cumulative burden of chronic stress and life events. It involves the interaction of different physiological systems at varying degrees of activity. When environmental challenges exceed the individual ability to cope, then allostatic overload ensues. Allostatic load is identified by the use of biomarkers and clinical criteria. Objective: To summarize the current knowledge on allostatic load and overload and its clinical implications based on a systematic review of the literature. Methods: PubMed, PsycINFO, Web of Science, and the Cochrane Library were searched from inception to December 2019. A manual search of the literature was also performed, and reference lists of the retrieved articles were examined.We considered only studies in which allostatic load or overload were adequately described and assessed in either clinical or non-clinical adult populations. Results: A total of 267 original investigations were included. They encompassed general population studies, as well as clinical studies on consequences of allostatic load/overload on both physical and mental health across a variety of settings. Conclusions: The findings indicate that allostatic load and overload are associated with poorer health outcomes. Assessment of allostatic load provides support to the understanding of psychosocial determinants of health and lifestyle medicine. An integrated approach that includes both biological markers and clinimetric criteria is recommended.

Background Discrimination promotes multisystem physiological dysregulation termed allostatic load, which predicts morbidity and mortality. It remains unclear whether weight-related discrimination influences allostatic load. Purpose The aim of this study was to prospectively examine 10-year associations between weight discrimination, allostatic load, and its components among adults 25–75 years in the Midlife Development in the US Biomarker Substudy. Methods Participants with information on weight discrimination were analyzed ( n =986). At both timepoints, participants self-reported the frequency of perceived weight discrimination across nine scenarios as “never/rarely” (scored as 0), “sometimes” (1), or “often” (2). The two scores were averaged and then dichotomized as “experienced” versus “not experienced” discrimination. High allostatic load was defined as having ≥3 out of 7 dysregulated systems (cardiovascular, sympathetic/parasympathetic nervous systems, hypothalamic pituitary axis, inflammatory, lipid/metabolic, and glucose metabolism), which collectively included 24 biomarkers. Relative risks (RR) were estimated from multivariate models adjusted for sociodemographic and health characteristics, other forms of discrimination, and BMI. Results Over 41% of the sample had obesity, and 6% reported weight discrimination at follow-up. In multivariable-adjusted analyses, individuals who experienced (versus did not experience) weight discrimination had twice the risk of high allostatic load (RR, 2.07; 95 % CI, 1.21; 3.55 for baseline discrimination; 2.16, 95 % CI, 1.39; 3.36 for long-term discrimination). Weight discrimination was associated with lipid/metabolic dysregulation (1.56; 95 % CI 1.02, 2.40), glucose metabolism (1.99; 95 % CI 1.34, 2.95), and inflammation (1.76; 95 % CI 1.22, 2.54), but no other systems. Conclusions Perceived weight discrimination doubles the 10-year risk of high allostatic load. Eliminating weight stigma may reduce physiological dysregulation, improving obesity-related morbidity and mortality.

Critical-grade insults (CGIs), such as sepsis, pose extreme challenges to host homeostasis. Although unfavorable immune responses in these conditions are commonly described as dysregulated, such perturbations are often defined retrospectively based on clinical outcomes rather than on the underlying immune processes. Here, I propose that, particularly in its early phase, the immune system response to sepsis reflects a high-stakes host response aimed at rapid control of the insult, albeit one that carries substantial risk to the host. If the inciting challenge is effectively contained, the immune response may resolve and transition toward tissue repair and recovery. Conversely, failure to control the insult may result in host death. In this context, the early immune response can be conceptualized within a “win versus loss” framework, where win is described as the ability to control inciting insult, while loss is host demise. Consequently, the term “dysregulation” may not fully capture the probabilistic feature of the initial response. Rather than representing a simple failure of control, this response may reflect an aggressive but potentially hazardous strategy that, in some cases, proves unsuccessful. Timely medical interventions, including appropriate antibiotic therapy, source control, or immunological endotype-based strategies, can modify CGI immunological trajectory by limiting insult burden and reducing the duration and intensity of the host response, thereby improving the likelihood of survival. Nevertheless, sustained or excessive early immune activation may disrupt regulatory networks, resulting in inevitable demise in some individuals, while others will exhibit an emergence of maladaptive allostatic states that can impair full recovery.

In this paper, we integrate recent theoretical and empirical developments in predictive coding and active inference accounts of interoception (including the Embodied Predictive Interoception Coding model) with working hypotheses from the theory of constructed emotion to propose a biologically plausible unified theory of the mind that places metabolism and energy regulation (i.e. allostasis), as well as the sensory consequences of that regulation (i.e. interoception), at its core. We then consider the implications of this approach for understanding depression. We speculate that depression is a disorder of allostasis, whose myriad symptoms result from a ‘locked in’ brain that is relatively insensitive to its sensory context. We conclude with a brief discussion of the ways our approach might reveal new insights for the treatment of depression. This article is part of the themed issue ‘Interoception beyond homeostasis: affect, cognition and mental health’.

In the last two decades, neuroscience studies have suggested that various psychological phenomena are produced by predictive processes in the brain. When considered together, these studies form a coherent, neurobiologically inspired program for guiding psychological research about the mind and behavior. In this article, we consider the common assumptions and hypotheses that unify an emerging framework and discuss the ramifications of such a framework, both for improving the replicability and robustness of psychological research and for renewing psychological theory by suggesting an alternative ontology of the human mind.

Achieving ambitious goals in Global Health first requires an integrative understanding of how individuals and organizations adapt in a living ecosystem. The absence of a unified framework limits the consideration of the issues in their complexity, which further complicates the planning of Global Health programs aimed at articulating population-based prevention and individual-level (clinical) interventions. The aim of the conceptual contribution is to propose such a model. It introduces the Dynamic Ecosystem of Adaptation through Allostasis (DEA-A) theoretical framework, emphasizing the functional adaptation of individuals and organizations in symbiosis with their living ecosystem. The DEA-A framework articulates two central components to grasp the complexity of adaptation: the internal dynamics (intrasystem level) and the environmental dynamics (ecosystem level). It bridges diverse conceptual approaches, including stress and adaptation models, behavior-change models, and ecosystem-based perspectives. Epistemological considerations raised in the conceptual article prompt a reconsideration of methods and tools for the planning of intervention. Further contributions will present a suitable methodology for the application of the DEA-A framework along with practical recommendations.