PMC:7795888 / 1710-6881 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/7795888","sourcedb":"PMC","sourceid":"7795888","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7795888","text":"1. Introduction\nThe COVID-19 pandemic and the resulting isolation have spiked stress-related symptoms worldwide [1]. Italy was the first European Country to face the COVID-19 emergency and to declare a national lockdown [2]. On 9 March 2020, the Italian government imposed a national quarantine, restricting the movement of the population except for necessity, special work permissions, and health conditions. Preventive containment measures during the COVID-19 epidemic, including self-isolation and social distancing, had a strong impact on people’s daily life and adversely affected psychological well-being further.\nIndividuals experiencing stress symptoms can feel overwhelmed with emotions and can be at higher risk for developing clinical depressive symptoms. However, only mixed evidence is available for whether inter-individual characteristics and demographics may account for determining the psychological response of a population facing massive stressful events [3]. Hence, as the epidemic continues, enhancing our ability to detect possible predictors of the psychological impact during the COVID-19 outbreak is an important focus point.\n“Anhedonia” is derived from the Greek “a-” (without) “hedone” (pleasure, delight) and is described as the inability to gain pleasure from normally pleasurable activities. Pleasure plays a key role in predisposing survival of biological resources and in guaranteeing an essential contribution to the success of adaptive behaviors [4]. Conversely, anhedonia is an obstacle to achieving evolutionary goals, and it has been considered as a core feature of depressive phenotypes [5], insomuch that Klein proposed the existence of a subtype of major depression, referred to as endogenomorphic depression, marked by characterological anhedonic features [6]. Indeed, anhedonia is a required symptom for the diagnosis of a major depressive episode, and evidence suggests that trait anhedonia may represent an important prognostic indicator in individuals suffering from affective disorders [7]. Differences in anhedonia have also been studied on an individual level, suggesting that the subjective hedonic experience originates from brain areas that activate to drive us toward the attainment of primary or secondary human needs [8]. These regions are part of the so-called brain reward system: amygdala, nucleus accumbens, orbitofrontal cortex (OFC), and cingulate cortex. In particular, Zhang et al. [9] suggested that the morphology of the OFC reflects quantitative traits of anhedonia that are continuously distributed throughout the general population and may serve to identify subjects who are at enhanced risk of developing affective disorders.\nEmotional responses are multifaceted phenomena that are associated with bodily symptoms, subjective experiences, cognitive changes, and action tendencies, whereas the hedonic marking of emotions is the quality that distinguishes affects from other psychological processes [10]. Research on emotion regulation has highlighted that individuals actively respond and often try to modify their affective states rather than passively experience them. Indeed, emotion regulation broadly refers to the ability to monitor and evaluate emotional experiences, modulate their intensity or duration, and adaptively manage emotional reactions in order to meet situational demands [11]. A substantial body of literature suggests the role of emotion dysregulation in accounting for the onset, overlap, and maintenance of depression [12]. Studies examining emotion regulation in depression have also suggested that depressed individuals exhibit more frequent use of maladaptive strategies, including suppression and rumination, when regulating affects and show difficulties effectively implementing adaptive strategies [13].\nThe documented connection between epidemics and mental health sequelae dates back more than 100 years ago, when Menninger associated the 1918 Spanish flu pandemic with psychiatric morbidity [14].\nOver the past few months, a number of studies reported on the prevalence of depressive symptoms among the general population during the COVID-19 pandemic and identified several potential predictive factors, including age, gender, marital status, education level, occupation, loneliness, having an acquaintance infected with COVID-19, as well as past history of medical disorders [15,16,17]. Conversely, relatively few studies have investigated psychological determinants of depressive symptoms severity during the COVID-19 outbreak [18,19,20,21].\nIn light of these observations, we aimed at filling this gap by reporting prevalence of depressive symptoms and distribution patterns of hedonic and emotional dysregulation in a sizeable sample of 500 healthy individuals assessed in the early phase of the COVID-19 outbreak in Italy. Further, we sought to identify risk factors predicting depression severity among demographic characteristics, medical and psychopathological variables, and information on lockdown conditions. We hypothesized that reduced hedonic capacity and emotional dysregulation might specifically predict depression severity during the COVID-19 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