Urbanization is reshaping global health, with over 55% of the world’s population residing in urban areas, a figure projected to reach 68% by 2050. This demographic shift presents significant challenges and opportunities for public health, as urban environments exacerbate health disparities rooted in social determinants of health, such as economic stability, education, neighborhood conditions, and access to healthcare. Rapid urban growth, particularly in low- and middle-income countries, has led to the emergence of inequitable living conditions, environmental hazards, and limited access to essential health services, contributing to the early onset of multimorbidity and rising non-communicable disease burdens. Urbanization-driven factors such as obesogenic environments, sedentary lifestyles, air pollution, and inadequate sleep exacerbate cardiovascular and metabolic risks, while social exclusion, overcrowding, and inadequate mental health services heighten vulnerabilities. Emerging risks, including urban heat islands, noise pollution, and exposure to endocrine-disrupting chemicals, further compound urban health inequities. Effective mitigation requires multi-sectoral policies that prioritize health-promoting infrastructure, reduce environmental pollutants, foster equitable healthcare access, and address systemic barriers affecting marginalized groups. This review explores the intersections between urbanization and health inequities, emphasizing the importance of addressing traditional and emerging risk factors across the lifespan. Policy implications include promoting green infrastructure, enhancing urban mobility, expanding mental health care, and leveraging participatory governance to foster resilient and inclusive cities. By adopting an integrated approach that prioritizes social equity and sustainability, cities can mitigate health disparities and create healthier, more inclusive urban environments that support the well-being of all residents.

Muscle strength is a relevant metric of aging. Greater adherence to Mediterranean diet is associated with better health outcomes across all life stages; however, evidence on the relationship between Mediterranean diet and muscle strength in older adults is inconclusive. In this study, we evaluated the relationship between adherence to Mediterranean diet and handgrip strength in a large sample of community-dwelling older adults from the Longevity Check-up 7+ project. A total of 2963 participants (mean age 72.8 ± 5.7 years; 54.4% women) were analyzed. Mediterranean diet adherence was evaluated using a modified Medi-Lite score and categorized as low (≤8), good (9 to 11), or high (≥12). Handgrip strength was categorized as normal or low according to cut-points by the European Working Group on Sarcopenia in Older People 2. Older adults with lower Mediterranean diet adherence had a significantly higher prevalence of probable sarcopenia (25.9%) than those with good (19.1%) or high (15.5%) adherence. The proportion of participants with probable sarcopenia increased with age, but it remained lower in the good and high adherence groups. Logistic regression showed that greater Mediterranean diet adherence was associated with a lower risk of probable sarcopenia. Older age, female sex, and physical inactivity were associated with a greater risk of probable sarcopenia. Our findings emphasize the positive association between healthy lifestyles, including adherence to Mediterranean diet, and physical function in old age.

Background: Sarcopenia is characterized by the progressive loss of skeletal muscle mass, strength, and function, significantly impacting overall health and quality of life in older adults. This narrative review explores emerging targets and potential treatments for sarcopenia, aiming to provide a comprehensive overview of current and prospective interventions. Methods: The review synthesizes current literature on sarcopenia treatment, focusing on recent advancements in muscle regeneration, mitochondrial function, nutritional strategies, and the muscle–microbiome axis. Additionally, pharmacological and lifestyle interventions targeting anabolic resistance and neuromuscular junction integrity are discussed. Results: Resistance training and adequate protein intake remain the cornerstone of sarcopenia management. Emerging strategies include targeting muscle regeneration through myosatellite cell activation, signaling pathways, and chronic inflammation control. Gene editing, stem cell therapy, and microRNA modulation show promise in enhancing muscle repair. Addressing mitochondrial dysfunction through interventions aimed at improving biogenesis, ATP production, and reducing oxidative stress is also highlighted. Nutritional strategies such as leucine supplementation and anti-inflammatory nutrients, along with dietary modifications and probiotics targeting the muscle–microbiome interplay, are discussed as potential treatment options. Hydration and muscle–water balance are emphasized as critical in maintaining muscle health in older adults. Conclusions: A combination of resistance training, nutrition, and emerging therapeutic interventions holds potential to significantly improve muscle function and overall health in the aging population. This review provides a detailed exploration of both established and novel approaches for the prevention and management of sarcopenia, highlighting the need for further research to optimize these strategies.

Coronary artery disease (CAD) is highly prevalent in older adults, yet its management remains challenging. Treatment choices are made complex by the frailty burden of older patients, a high prevalence of comorbidities and body composition abnormalities (e.g., sarcopenia), the complexity of coronary anatomy, and the frequent presence of multivessel disease, as well as the coexistence of major ischemic and bleeding risk factors. Recent randomized clinical trials and epidemiological studies have provided new data on optimal management of complex patients with CAD. However, frail older adults are still underrepresented in the literature. This narrative review aims to highlight the importance of assessing frailty as an aid to guide therapeutic decision-making and tailor CAD management to the specific needs of older adults, taking into account age-related pharmacokinetic and pharmacodynamic changes, polypharmacy, and potential drug interactions. We also discuss gaps in the evidence and offer perspectives on how best in the future to optimize the global strategy of CAD management in older adults.

Hip fractures are among the most serious health events in older adults, frequently leading to disability, loss of independence, and elevated mortality. In 2019, an estimated 9.6 million new cases occurred globally among adults aged ≥ 55 years, with an incidence rate of 681 per 100,000. Despite improved surgical care, one-year mortality remains high (15–30%), and fewer than half of survivors regain their pre-fracture functional status. Traditionally regarded as mechanical injuries, hip fractures are now increasingly recognized as systemic events reflecting and accelerating biological vulnerability and frailty progression. We synthesize evidence across biological, clinical, and social domains to explore the systemic implications of hip fracture, from the acute catabolic response and immune dysfunction to long-term functional decline. The concept of intrinsic capacity, introduced by the World Health Organization, offers a resilience-based framework to assess the multidimensional impact of hip fracture on physical, cognitive, and psychological function. We highlight the importance of orthogeriatric co-management, early surgical intervention, and integrated rehabilitation strategies tailored to the individual’s functional reserves and personal goals. Innovations such as digital health tools, biological aging biomarkers, and personalized surgical approaches represent promising avenues to enhance recovery and autonomy. Ultimately, we advocate for a shift toward interdisciplinary, capacity-oriented models of care that align with the goals of healthy aging and enable recovery that transcends survival, focusing instead on restoring function and quality of life.

Chronic inflammation is a pivotal driver in the progression of atherosclerosis, significantly contributing to the burden of cardiovascular disease (CVD). Patients with chronic inflammatory diseases, such as inflammatory bowel diseases (IBDs) (e.g., ulcerative colitis and Crohn’s disease), rheumatological disorders, as well as individuals with auto-immune diseases (such as systemic lupus erythematosus), present a higher risk of major adverse cardiac events (MACEs). Despite their elevated CVD risk, these populations remain underrepresented in cardiovascular research, leading to a critical underestimation of their cardiovascular risk (CVR) in clinical practice. Furthermore, even recent CVR scores poorly predict the risk of events in these specific populations. This narrative review examines the physiopathological mechanisms linking chronic inflammation, immunomodulation, atherosclerosis, thrombosis and cardiovascular events. We review data from epidemiological studies and clinical trials to explore the potential cardiovascular benefits of anti-inflammatory and immunomodulatory therapies. Despite existing evidence, significant gaps in knowledge remain. Future research is mandatory, focusing on innovative strategies for risk stratification and optimization, including lipidomics, proteomics, advanced inflammatory markers, microbiota profiling, and cardiovascular imaging. Addressing these unmet needs will enhance understanding of cardiovascular risk in chronic inflammatory diseases, enabling tailored interventions and better outcomes.