Psoriasis is a chronic immune-mediated skin disease characterized by cytokine dysregulation. Pro-inflammatory mediators, including tumor necrosis factor-alpha (TNF-α), interleukin (IL)-17, and IL-23, play pivotal roles in the pathogenesis of psoriasis. Emerging evidence suggests that dietary interventions can modulate cytokine activity, providing a complementary approach to standard therapies. This narrative review examines the impact of various dietary strategies, including a Mediterranean diet, ketogenic diet, gluten-free diet, and fasting-mimicking diet, on cytokine profiles and clinical outcomes in psoriasis. Research insights reveal that dietary components such as omega-3 fatty acids, polyphenols, and short-chain fatty acids influence immune signaling pathways. These pathways include nuclear factor-kappa B (NF-κB) and Signal Transducer and Activator of Transcription 3 (STAT3). Additionally, these dietary components promote anti-inflammatory effects mediated by gut microbiota. Clinical studies demonstrate significant reductions in psoriasis severity, improved quality of life, and modulation of key cytokines associated with disease activity. Despite these advancements, significant challenges persist in effectively integrating these findings into clinical practice. These challenges include variability in patient responses, adherence issues, and the need for robust biomarkers to monitor efficacy. Future directions emphasize the potential of personalized nutrition and precision medicine approaches to optimize dietary interventions tailored to individual cytokine profiles and genetic predispositions. Integrating these strategies into psoriasis care could transform treatment paradigms by simultaneously addressing both systemic inflammation and comorbid conditions.

This narrative review analyzes how myokines act as key links in communication between skeletal muscle and the brain, focusing on the impact of aging on this axis. Although the current literature links defects in this signaling pathway to sarcopenia, neurodegeneration, and cognitive decline, we still do not know exactly what role each molecule plays individually. Among the main gaps in our understanding are questions about how these substances are transported to the nervous system, what their specific receptors are, and what cause-and-effect relationship actually exists between losing muscle mass and developing neurological problems. In fact, in humans, it remains unclear whether myokines actually reach the brain in truly effective concentrations or whether their benefits are due more to peripheral metabolic, vascular, and inflammatory changes. Today, most of the mechanistic evidence comes from animal and cellular models, while observational studies predominate in humans. This is further complicated by uncertainties regarding the actual origin of these proteins in tissues, their passage through the blood–brain barrier, and their measurement in the blood, making it difficult to determine whether these proteins act as causes, consequences, or simply compensatory responses to aging and disease. On the other hand, although exercise remains the most robust tool for maintaining muscle health and protecting cognitive function, it is still unclear whether we could replicate those same benefits by isolating and stimulating specific myokines. The major challenge for the future is to develop human studies that combine standardized biomarkers with long-term monitoring of muscle function, cognition, and brain structure. Only then will we know whether this fascinating muscle–brain axis can move beyond being a promising hypothesis to become a real therapeutic target.

Obesity care increasingly requires outcomes that extend beyond total body weight. Although weight reduction remains clinically meaningful, the scale alone does not indicate whether fat mass, lean tissue, muscle quality, strength, mobility, or physiological reserve have changed in a favorable direction. This narrative review examines the combined role of higher-protein dietary strategies and concurrent exercise in adults with obesity, with emphasis on body composition, metabolic health, and physical function. Higher-protein dietary strategies may support satiety, improve the tolerability of energy restriction in some patients, and attenuate lean-tissue loss during weight reduction, while evidence for superior long-term weight loss remains inconsistent. Exercise provides complementary stimuli to protein-focused nutrition: resistance training supports strength, muscle function, and lean-tissue preservation, while aerobic and interval-based training contribute to cardiorespiratory fitness, regional adiposity reduction, and selected cardiometabolic adaptations. Concurrent training offers a practical framework for integrating these stimuli, with value primarily as multidomain coverage rather than as evidence of universal superiority over other modalities. The main rationale for combining protein adequacy with exercise is preservation of usable physical function during weight loss, particularly in older adults, patients with sarcopenic-obesity risk, and individuals undergoing rapid pharmacological or surgical weight reduction. Overall, the available evidence is most consistent with viewing higher-protein nutrition and structured exercise as complementary strategies for improving the quality of weight loss, rather than as a single protocol for maximizing scale-weight reduction. Longer pragmatic trials are needed to clarify phenotype-specific responses, feasible protein targets, exercise progression, monitoring strategies, and functional outcomes.