Transitioning from childhood into adolescence is an extraordinary time of life, associated with major physical, emotional, cognitive, and social changes and characterized by dynamic development in which interaction with the environment modulates the individual resources responsible for well-being and health. This sensitive period is the time when, in addition to hormonal, metabolic, and neural changes, certain behavioral strategies begin to take shape that will shortly go on to define the emotional, social, and cultural identity of the individual. This narrative review aimed to uncover the crucial processes underlying the transition by identifying processes that are responsible for cognitive, psychosocial, and emotional development, in the absence of disease. For this aim, we highlight (1) the physical, psychological, and social determinants during the transition from childhood to adolescence; (2) the role of health-related variables in resilience or vulnerability mechanisms; and (3) recent school-based strategies to promote health and well-being. Recognizing that health and well-being are the result of the interaction of many biological, psychological, social, cultural, and physical factors will lead to comprehensive health promotion involving all actors joining the growth process, from health professionals and the educational community to parents and community. Furthermore, it is important that psychosocial dimensions are strengthened already during childhood to prevent the onset of frailty and illness in adolescence.

The prolonged lockdown imposed to contain the COrona VIrus Disease 19 COVID-19 pandemic prevented many people from direct contact with nature and greenspaces, raising alarms for a possible worsening of mental health. This study investigated the effectiveness of a simple and affordable remedy for improving psychological well-being, based on audio-visual stimuli brought by a short computer video showing forest environments, with an urban video as a control. Randomly selected participants were assigned the forest or urban video, to look at and listen to early in the morning, and questionnaires to fill out. In particular, the State-Trait Anxiety Inventory (STAI) Form Y collected in baseline condition and at the end of the study and the Part II of the Sheehan Patient Rated Anxiety Scale (SPRAS) collected every day immediately before and after watching the video. The virtual exposure to forest environments showed effective to reduce perceived anxiety levels in people forced by lockdown in limited spaces and environmental deprivation. Although significant, the effects were observed only in the short term, highlighting the limitation of the virtual experiences. The reported effects might also represent a benchmark to disentangle the determinants of health effects due to real forest experiences, for example, the inhalation of biogenic volatile organic compounds (BVOC).

The triad formed by thyroid dysfunction, metabolic syndrome (MetS), and cardiovascular (CV) risk forms a network with many connections that aggravates health outcomes. Thyroid hormones (THs) play an important role in glucose and lipid metabolism and hemodynamic regulation at the molecular level. It is noteworthy that a bidirectional association between THs and MetS and their components likely exists as MetS leads to thyroid dysfunction, whereas thyroid alterations may cause a higher incidence of MetS. Thyroid dysfunction increases insulin resistance, the circulating levels of lipids, in particular LDL-C, VLDL-C, and triglycerides, and induces endothelial dysfunction. Furthermore, THs are important regulators of both white and brown adipose tissue. Moreover, the pathophysiological relationship between MetS and TH dysfunction is made even tighter considering that these conditions are usually associated with inflammatory activation and increased oxidative stress. Therefore, the role of THs takes place starting from the molecular level, then manifesting itself at the clinical level, through an increased risk of CV events in the general population as well as in patients with heart failure or acute myocardial infarction. Thus, MetS is frequently associated with thyroid dysfunction, which supports the need to assess thyroid function in this group, and when clinically indicated, to correct it to maintain euthyroidism. However, there are still several critical points to be further investigated both at the molecular and clinical level, in particular considering the need to treat subclinical dysthyroidism in MetS patients.

In the last few years, many studies have focused on the effects of environmental contaminant exposure during the prenatal period or infancy as predictors of health outcomes in the future. In these time windows, due to their rapid growth, and physiologic and metabolic development, we can observe a higher vulnerability to the effects of environment, with respect to adulthood. The evidence of possible influences, partly mediated by epigenetic mechanisms, involve neurobehavioral responses and immune, endocrine, and respiratory systems, acting directly on the child or indirectly when mediated by placental transfer or breast feeding. In particular, due to a greater intake of air, food, and fluids relative to body weight, crawling behaviors and short stature, the risk of excessive exposure is greater in children. However, data on the long-term implications of early exposures are scarce. Additionally, so that physicians and institutions for child care and assistance of pregnant women can take actions to counteract the effects of chemical pollution (i.e., by educational opportunities), a risk assessment perspective that responds to the biocomplexity of the human being is needed. The present paper provides an overview of physiologic and behavioral characteristics during the perinatal period and in childhood, suggesting in a more integrated way, the need of a new risk-assessment approach to managing chronic disease in pediatric patients.

Background: Oxidative stress is crucial in the pathogenesis of atherosclerosis and acute myocardial infarction (AMI). Under the generic terms “oxidative stress” (OS), many biomarkers belonging to different pathways have been proposed. Aim: To compare the levels of recently proposed OS-related parameters in acute coronary syndromes (ACS) and stable coronary artery disease (CAD), to evaluate their effectiveness as additive risk or illness indicators of stable and acute ischemic events, and their response over time during the course of AMI. Methods: 76 ACS, 77 CAD patients, and 63 controls were enrolled in the study. Different OS-related biomarkers, including reactive oxygen metabolites (ROM), the total antioxidant capacity (OXY), nitrite/nitrate (final nitric oxide products, NO_x), and Lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1), were evaluated. Moreover, time response during AMI course (admission, and 6, 12, 18, 24, 36, and 48 hours after, T0-T6, respectively) and correlation with traditional cardiovascular (CV) risk factors (age, gender, hypertension, diabetes mellitus, dyslipidemia, smoking habit) were also assessed. Results: Over time, ROM progressively increased while OXY and NO_x decreased. Kinetics of LOX-1 during AMI shows that this biomarker boosts early during the acute event (T1 and T2) and then progressively decreases, being significantly lower from T0 to T6. Different OS-related biomarkers were differentially associated with CV risk factors and CAD or ACS presence. Conclusion: Differences in OS-related biomarkers (between groups, according to the response over time during AMI, and to the presence of CV risk factors) confirmed OS involvement in the transition from healthy status to stable CAD and ACS, although evidencing the heterogeneous nature of redox processes. In future, a multi-marker panel including different biomarkers and pathways of oxidative stress could be evaluated as an additive tool to be used in the CV prevention, diagnosis, patient stratification, and treatment.

Physiological stressors, such as exercise, can precipitate sudden cardiac death or heart failure progression in patients with arrhythmogenic cardiomyopathy (ACM). Yet, whether and to what extent a highly prevalent and more elusive environmental factor, such as psychosocial stress (PSS), can also increase ACM disease progression is unexplored. Here, we first quantified perceived stress levels in patients with ACM and found these levels correlated with the extent of arrhythmias and cardiac dysfunction. To determine whether the observed correlation is due to causation, we inflicted PSS-via the resident-intruder (RI) paradigm—upon Desmoglein-2 mutant mice, a vigorously used mammalian model of ACM. We found that ACM mice succumbed to abnormally high in-trial, PSS mortality. Conversely, no sudden deaths occurred in wildtype (WT) counterparts. Desmoglein-2 mice that survived RI challenge manifested markedly worse cardiac dysfunction and remodeling, namely apoptosis and fibrosis. Furthermore, WT and ACM mice displayed similar behavior at baseline, but Desmoglein-2 mice exhibited heightened anxiety following RI-induced PSS. This outcome correlated with the worsening of cardiac phenotypes. Our mouse model demonstrates that in ACM-like subjects, PSS is incisive enough to deteriorate cardiac structure and function per se, i.e., in the absence of any pre-existing anxious behavior. Hence, PSS may represent a previously underappreciated risk factor in ACM disease penetrance.