The high prevalence of multiple comorbidities poses unique medication-related challenges for geriatric patients. Polypharmacy is a particular concern since taking several medications simultaneously increases the likelihood of adverse drug events and the risk of drug interactions while decreasing patient adherence. These factors are associated with suboptimal health outcomes and a heightened burden on the healthcare system (insurance claims) and the patient (out-of-pocket expenses). These challenges can significantly affect the quality of life of geriatric patients. This chapter critically examines the impact of medication use and polypharmacy on the quality of life of older patients. In addition, the authors discuss how artificial intelligence-based digital tools and precision medicine can address these issues by streamlining medical decision-making, improving the patient experience, and allowing remote monitoring. Finally, they interpret the findings from the lens of ethical considerations associated with the adoption and implementation of digital applications and gadgets. Request access from your librarian to read this chapter's full text.

Hypertension (HTN) and chronic kidney disease (CKD) are significant global health burdens, with microalbuminuria (MA) serving as a key early marker of renal damage and cardiovascular risk. While nutritional interventions are pivotal for management, the evidence for specific nutrients is often complex and inconsistent, creating challenges for clinical guidance. This review critically evaluates current evidence on the interaction among macronutrients, micronutrients, and established dietary approaches and their influence on the development and course of HTN and MA. Strong consensus is present regarding sodium restriction, increased intakes of potassium, and the implementation of dietary patterns like Dietary Approaches to Stop Hypertension (DASH) and the Mediterranean diet to improve blood pressure and renal outcomes. Evidence favors protein moderation (approximately 0.8 g/kg/day), especially from plant sources, and emphasizes carbohydrate quality (e.g., high fiber, low glycemic index) over absolute quantity. The role of micronutrients is more nuanced; maintaining vitamin D sufficiency is protective, but intervention trials for many supplements, including B vitamins and antioxidant vitamins (C and E), have yielded inconsistent results. Several minerals, such as iron and selenium, exhibit a U-shaped risk curve where both deficiency and excess are detrimental, highlighting the risks of unselective supplementation. Ideal nutrition care prioritizes holistic dietary patterns over a focus on single nutrients. Clinical guidance should be founded on sodium reduction and potassium-rich foods, with personalized recommendations for protein and micronutrient supplementation based on an individual’s specific cardiovascular and renal profile. Future research must target nutrients with conflicting evidence to establish clear, evidence-based intake guidelines.

Stromal cell‐derived factor‐1α (SDF‐1α) is a potent stem cell recruitment chemokine that can promote angiogenesis, particularly when delivered via gene‐activated scaffolds (GAS). This systematic review and meta‐analysis synthesized in vitro evidence on the angiogenic potential of SDF‐1α GAS. Four databases were utilized to search for eligible studies, comprising investigations that examined the in vitro effects of SDF‐1α GAS on angiogenesis‐related outcomes compared with gene‐free scaffolds. Data on gene expression, protein levels, and endothelial formation were extracted. Meta‐analyses were conducted using random or fixed‐effect models, expressed as standardized mean difference (SMD) or mean difference (MD) with 95% confidence intervals (CI). Risk of bias was assessed using the Quality Assessment Tool for In Vitro Studies (QUIN) tool. Eight studies were included. Pooled analysis demonstrated SDF‐1α GAS efficacy to significantly increase SDF‐1α gene expression (SMD = 1.20; 95% CI = 0.13–2.27; p = .03), fold‐change of the gene (MD = 12.48; 95% CI = 10.33–14.64; p < .0001), and protein production (MD = 0.29 ng/mL; 95% CI = 0.14–0.43 ng/mL; p = .0001). Most studies showed a moderate risk of bias. Based on in vitro studies, SDF‐1α GAS activity is associated with significant elevation of SDF‐1α gene expression and protein quantity, although it did not exhibit significant enhancement of VEGF expression or functional endothelial morphogenesis under the studied conditions.

Aim To analyze the effect of vitamin D administration on serum 25(OH)D levels and biomarkers of metabolic syndrome and atherosclerosis (homeostatic model assessment of insulin resistance [HOMA-IR], adiponectin, homocysteine, and high sensitivity C-reactive protein [hs-CRP]) in epilepsy patients receiving enzymatic antiseizure medications (ASMs). Methods This double-blind, randomized, placebo-controlled trial randomized 40 adult epilepsy patients treated with enzymatic ASMs to receive vitamin D3 (2,000 IU/day) or placebo for 12 weeks. The primary outcome was the change in serum 25-hydroxyvitamin D (25[OH]D) levels. Secondary outcomes included changes in HOMA-IR, adiponectin, homocysteine, and hs-CRP. Data were analyzed using a per-protocol approach. Results Thirty-four patients completed the study. Vitamin D supplementation yielded a significantly greater increase in serum 25(OH)D (10.67 ± 8.16 vs. –1.29 ± 3.96 ng/mL; p < 0.001) and adiponectin (1.38 ± 3.05 vs. 0.34 ± 1.89 µg/mL; p = 0.045), as well as a significantly greater reduction in hs-CRP (–6.74 ± 14.65 vs. 1.81 ± 7.75 mg/L; p = 0.041) compared with placebo. Conversely, no significant differences were observed between groups regarding the changes in HOMA-IR (–0.24 ± 3.71 vs. –0.14 ± 3.38; p = 0.940) or homocysteine (7.90 ± 1.79 vs. 8.15 ± 2.70 µmol/L; p = 0.290). Conclusion Vitamin D supplementation (2,000 IU/day) effectively restores 25(OH)D levels and improves adiponectin and hs-CRP in epilepsy patients on enzymatic ASMs, suggesting a potential benefit for cardiovascular risk reduction. However, vitamin D alone did not prevent the rise in homocysteine, likely due to the concurrent cessation of B-vitamin supplementation.