Overnutrition is a predominant issue in contemporary society, increasing rapidly despite considerable progress in our comprehension of nutrition, the health consequences of different food categories, and the dangers linked to excessive calorie consumption. The pathways connecting obesity to associated disorders are intricate, although research has consistently identified oxidative stress as a principal facilitator of the progression of many diseases. In this paper, the synthesis of various reactive species at the molecular level is studied, and the influence of diet on their production is assessed, with a thorough examination of the cellular mechanisms involved. Furthermore, the correlation between oxidative stress and the development of cardiometabolic diseases is explored, highlighting the most recent and relevant research in the field.

As accumulated evidence suggests that individuals with post-traumatic stress disorder (PTSD) encounter earlier and more frequent occurrences of cardiovascular diseases, the aim of this study was to ascertain the differences in lifestyle and cardiovascular risk between PTSD and complex PTSD patients. We enrolled 137 male war veterans with PTSD (89 had complex PTSD). The diagnosis was established based on 11th revision of International Classification of Diseases (ICD-11), and cardiovascular risk was estimated by the measurement of advanced glycation end products. Adherence to Mediterranean diet (MD) was lower in the complex PTSD group (2.2% vs. 12.5%, p = 0.015). Accordingly, patients with complex PTSD had lower healthy lifestyle scores in comparison to PTSD counterparts (50.6 ± 9.7 vs. 59.6 ± 10.1, p < 0.001), and a positive association was noted between MD adherence and a healthy lifestyle (r = 0.183, p = 0.022). On the other hand, differences were not noted in terms of physical activity (p = 0.424), fat % (p = 0.571) or cardiovascular risk (p = 0.573). Although complex PTSD patients exhibit worse adherence to MD and lower healthy lifestyle scores, these differences do not seem to impact physical activity, body composition, or estimated cardiovascular risk. More research is needed to clarify if this lack of association accurately reflects the state of the PTSD population or results from insufficient statistical power.

Background and Objectives: Handgrip strength (HGS) is a simple marker of muscular fitness that has been linked to adverse outcomes in older adults, while menopause is accompanied by skeletal deterioration and increased psychological vulnerability. Resilience and self-regulation may be associated with lower levels of these risks, but their relationship with bone microarchitecture has not been clarified. We aimed to examine the associations between HGS and trabecular bone score (TBS), bone mineral density (BMD), mental health, resilience, and self-regulation in postmenopausal women. Materials and Methods: In this study, 200 postmenopausal women were recruited. HGS was assessed with a dynamometer, BMD at the lumbar spine, total hip and femoral neck by DXA, and lumbar TBS was derived from spine images. Psychological distress was measured with the DASS-21, resilience with the Brief Resilience Scale (BRS), and self-regulation with the Short Self-Regulation Questionnaire (SSRQ). Results: TBS was significantly higher in women with higher HGS (p < 0.001). Higher HGS was also associated with lower anxiety and depression scores (p = 0.011 and p = 0.013), fewer self-reported mental health disorders, and greater resilience (p < 0.001) and self-regulation (p = 0.004). Resilience and self-regulation were inversely related to all DASS-21 subscales (all p < 0.001), and HGS correlated positively with BRS (p < 0.001) and SSRQ (p < 0.001). TBS correlated modestly with both BRS (p = 0.003) and HGS (p < 0.001). In multiple linear regression, both BRS (β = 0.018, p = 0.013) and HGS (β = 0.003, p = 0.006) remained independently associated with TBS after adjustment for age, BMI, menopause duration, and SSRQ. Conclusions: In postmenopausal women, higher handgrip strength is associated to better trabecular bone microarchitecture and a more favorable psychological profile. Incorporating HGS and brief psychosocial assessment alongside TBS may enrich fracture risk stratification and support more integrated musculoskeletal and mental health care.

Epidemiological studies suggest that, despite the adverse effects of excessive alcohol intake, low-to-moderate levels of wine consumption have been associated with favorable cardiovascular outcomes. While the biological effects of polyphenol-rich red wine have been extensively studied, less is known about the impact of white wine on myocardial cellular function and the underlying mechanisms. In this study, young male Sprague-Dawley rats were given ad libitum access to white wine or water for four weeks, after which cardiac mitochondrial function, cardiomyocyte susceptibility to oxidative stress, and cardiac transcriptomic profiles were assessed using respirometry, ROS measurements, in vitro oxidative stress assay, and RNA sequencing. White wine consumption did not significantly alter mitochondrial respiratory capacity, expression of antioxidant enzymes or cardiomyocyte survival following oxidative challenge. However, mitochondrial ROS production at respiratory complex I was significantly reduced, particularly during reverse electron transport mimicking ischemia/reperfusion. Transcriptomic analysis revealed modest changes, with no genes meeting the false discovery rate threshold. Analyses based on nominal significance revealed changes associated with mitochondrial electron transfer, protein quality control, apoptosis, and inflammatory signaling. In conclusion, four-week white wine consumption was associated with reduced mitochondrial ROS without impairing cardiac bioenergetics, accompanied by subtle transcriptional responses.