Alarming statistics show that the number of people affected by excessive weight has surpassed 2 billion, representing approximately 30% of the world’s population. The aim of this review is to provide a comprehensive overview of one of the most serious public health problems, considering that obesity requires an integrative approach that takes into account its complex etiology, including genetic, environmental, and lifestyle factors. Only an understanding of the connections between the many contributors to obesity and the synergy between treatment interventions can ensure satisfactory outcomes in reducing obesity. Mechanisms such as oxidative stress, chronic inflammation, and dysbiosis play a crucial role in the pathogenesis of obesity and its associated complications. Compounding factors such as the deleterious effects of stress, the novel challenge posed by the obesogenic digital (food) environment, and the stigma associated with obesity should not be overlooked. Preclinical research in animal models has been instrumental in elucidating these mechanisms, and translation into clinical practice has provided promising therapeutic options, including epigenetic approaches, pharmacotherapy, and bariatric surgery. However, more studies are necessary to discover new compounds that target key metabolic pathways, innovative ways to deliver the drugs, the optimal combinations of lifestyle interventions with allopathic treatments, and, last but not least, emerging biological markers for effective monitoring. With each passing day, the obesity crisis tightens its grip, threatening not only individual lives but also burdening healthcare systems and societies at large. It is high time we took action as we confront the urgent imperative to address this escalating global health challenge head-on.

Homocysteine (Hcy) is becoming a well-established risk factor for cardiovascular disease (CVD), mainly involving endothelial dysfunction and atherogenesis. Endothelial dysfunction is reflected primarily in the complex regulation of the main physiological and pathophysiological processes. There is increasing evidence regarding abnormally high concentrations of plasma total homocysteine, or plasma hyperhomocysteinemia, contributing to endothelial dysfunction, inflammation, and CVD. This clinical and experimental study examined the connection between Hcy and cardiovascular disease risk. Homocysteine is a marker of total vascular damage that must be monitored and controlled as early as possible. Dietary and lifestyle changes are recommended for most patients with hyperhomocysteinemia (Hhcy). The purpose of this paper is to review the data from the specialized literature that demonstrate that there is a direct link between endothelial injury and increased homocysteine levels, identifying existing evidence, describing new mechanisms, and exploring potential new therapeutic options. These aspects continue to be debated, and additional efforts are required to refine therapeutic strategies and to investigate the potential implications of Hcy in health and disease.

Childhood obesity is a major global health problem, and its management involves a multidisciplinary approach that includes lifestyle changes, dietary interventions, and the use of dietary supplements. In this review, we summarize current findings on the role of amino acids in pediatric obesity, with a particular focus on their involvement in metabolic pathways and weight regulation. The involvement of branched-chain and aromatic amino acids in the pathophysiology and potential management of pediatric obesity is highlighted in recent studies. Both experimental and clinical studies have shown that obese children often exhibit altered plasma amino acid profiles, including increased levels of leucine, isoleucine, valine, phenylalanine, and tyrosine, as well as decreased levels of glycine and serine. These imbalances are correlated with insulin resistance, inflammation, and early metabolic dysfunction. One of the mechanisms through which branched-chain amino acids can promote insulin resistance is the activation of the mammalian target of rapamycin (mTOR) signaling pathway. Metabolomic profiling has demonstrated the potential of specific amino acid patterns to predict obesity-related complications before they become clinically evident. Early identification of these biomarkers could be of great help for individualized interventions. Although clinical studies indicate that changes in dietary amino acids could lead to modest weight loss, improved metabolic profiles, and increased satiety, further studies are needed to establish standardized recommendations.

Atherosclerosis is still considered a disease burden with long-term damaging processes towards the cardiovascular system. Evaluation of atherosclerotic stages requires the use of independent markers such as those already considered traditional, that remain the main therapeutic target for patients with atherosclerosis, together with emerging biomarkers. The challenge is finding models of predictive markers that are particularly tailored to detect and evaluate the evolution of incipient vascular lesions. Important advances have been made in this field, resulting in a more comprehensible and stronger linkage between the lipidic profile and the continuous inflammatory process. In this paper, we analysed the most recent data from the literature studying the molecular mechanisms of biomarkers and their involvement in the cascade of events that occur in the pathophysiology of atherosclerosis.