Background: Chronic obstructive pulmonary disease (COPD) is a progressive, inflammatory airway disorder characterized by a gradual decline in lung function and increased oxidative stress. Both oxidative stress and inflammation are central to its pathophysiology, with trace elements such as zinc, copper, iron, manganese, magnesium, selenium, and calcium playing key roles in various cellular processes. Objective: This article reviews the role of trace elements in COPD, focusing on their involvement in disease pathogenesis and their therapeutic potential. Specifically, we examine the effects of zinc, copper, iron, magnesium, manganese, selenium, and calcium in COPD. Methods: We performed a comprehensive narrative review of the literature across databases including PubMed, Web of Science, Cochrane Library, and Google Scholar, identifying studies that explore the therapeutic effects of trace elements in COPD. The studies included in the review consisted of cohort analyses, randomized controlled trials, and clinical investigations. Results: Zinc, copper, iron, magnesium, manganese, selenium, and calcium are critical to both the pathophysiology and management of COPD. These trace elements contribute to the regulation of inflammation, the modulation of oxidative stress, and the maintenance of lung function. Zinc and copper, for instance, reduce oxidative stress and modulate immune responses, while iron is essential for oxygen transport. Magnesium, manganese, selenium, and calcium are vital for muscle function, respiratory performance, reducing inflammation, and improving pulmonary function. Conclusions: The minerals zinc, copper, iron, magnesium, manganese, selenium, and calcium may contribute to beneficial effects as part of the standard therapeutic management of COPD. Maintaining optimal levels of these trace elements may support the regulation of inflammatory processes, a reduction in oxidative stress, and an improvement in the pulmonary function. However, further clinical research is necessary to confirm their efficacy and establish safe dosage recommendations in COPD treatment.

Background: Accelerated demographic aging in Hungary and across Europe presents significant public health and socioeconomic challenges, particularly in preserving cognitive function and preventing neurodegenerative diseases. Modifiable lifestyle factors—especially dietary habits—play a critical role in brain aging and cognitive decline. Objective: This narrative review explores the mechanisms by which Western dietary patterns contribute to cognitive impairment and neurovascular aging, with specific attention to their relevance in the Hungarian context. It also outlines the rationale and design of the Semmelweis Study and its workplace-based health promotion program targeting lifestyle-related risk factors. Methods: A review of peer-reviewed literature was conducted focusing on Western diet, cognitive decline, cerebrovascular health, and dietary interventions. Emphasis was placed on mechanistic pathways involving systemic inflammation, oxidative stress, endothelial dysfunction, and decreased neurotrophic support. Key findings: Western dietary patterns—characterized by high intakes of saturated fats, refined sugars, ultra-processed foods, and linoleic acid—are associated with elevated levels of 4-hydroxynonenal (4-HNE), a lipid peroxidation product linked to neuronal injury and accelerated cognitive aging. In contrast, adherence to Mediterranean dietary patterns—particularly those rich in polyphenols from extra virgin olive oil and moderate red wine consumption—supports neurovascular integrity and promotes brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) activity. The concept of “cognitive frailty” is introduced as a modifiable, intermediate state between healthy aging and dementia. Application: The Semmelweis Study is a prospective cohort study involving employees of Semmelweis University aged ≥25 years, collecting longitudinal data on dietary, psychosocial, and metabolic determinants of aging. The Semmelweis–EUniWell Workplace Health Promotion Model translates these findings into practical interventions targeting diet, physical activity, and cardiovascular risk factors in the workplace setting. Conclusions: Improving our understanding of the diet–brain health relationship through population-specific longitudinal research is crucial for developing culturally tailored preventive strategies. The Semmelweis Study offers a scalable, evidence-based model for reducing cognitive decline and supporting healthy aging across diverse populations.

Background/Objectives: Population aging is accompanied by a rapidly increasing burden of neurodegenerative disorders, particularly Alzheimer’s and Parkinson’s diseases. Within the geroscience framework, targeting fundamental mechanisms of aging may delay the onset or progression of multiple age-related conditions. Dietary factors, especially plant-derived polyphenols, have gained increasing attention due to their potential to modulate molecular pathways involved in brain aging. This narrative review aims to integrate current evidence on dietary polyphenols and their role in modulating the molecular mechanisms underlying brain aging and neurodegeneration. Methods: This narrative review synthesizes findings from molecular, experimental, epidemiological, and clinical studies to provide an integrated assessment of the effects of dietary polyphenols on key cellular pathways involved in brain aging. Results: Polyphenols are widely present in plant-based foods, and polyphenol-rich dietary patterns—particularly the Mediterranean and MIND diets—have been consistently associated in observational studies with a reduced risk of cognitive decline. Mechanistic evidence, derived predominantly from in vitro and animal studies with limited validation in humans, suggests that polyphenols may influence key hallmarks of aging, including oxidative stress, chronic inflammation, mitochondrial dysfunction, cellular senescence, and impaired proteostasis. These effects are mediated through pathways such as Nrf2, NF-κB, AMPK, mTOR, and SIRT1, as well as via gut–brain axis interactions. However, clinical evidence remains heterogeneous. Conclusions: Dietary polyphenols represent a biologically plausible and promising, yet not fully validated, nutritional strategy for promoting healthy brain aging. Their translation into clinical practice is limited by low bioavailability, substantial interindividual variability, and the lack of large-scale, long-term randomized controlled trials.

Background: Ketogenic dietary therapies (KDTs), characterized by substantial carbohydrate restriction and increased dietary fat intake, were originally developed for the treatment of drug-resistant epilepsy but have recently attracted broader scientific interest. In the context of population aging and the increasing prevalence of cognitive impairment and dementia, their potential relevance for brain health has received growing attention. Experimental and emerging clinical evidence suggests that ketogenic metabolism may influence biological processes involved in brain aging, including cerebrovascular regulation, neuroinflammatory signaling, and cerebral energy metabolism. Objective: This narrative review aims to synthesize current evidence on the relationship between ketogenic dietary therapies and brain health, with particular emphasis on cerebrovascular mechanisms, neuroinflammatory pathways, and neuroprotective processes relevant to aging. The review also briefly introduces the Semmelweis Study as an example of a translational research framework for evaluating nutrition-related interventions in real-world preventive settings. Methods: A narrative literature review was conducted using structured searches of major scientific databases to identify experimental and human studies investigating ketogenic dietary interventions, cerebrovascular mechanisms, and neuroprotective outcomes. Publications related to the Semmelweis Study were included solely to illustrate implementation-oriented research approaches and not as evidence supporting dietary efficacy. Results: Available evidence indicates that ketogenic dietary interventions may modulate several biological pathways relevant to brain health, including cerebral energy metabolism, mitochondrial function, oxidative stress regulation, and inflammatory signaling. However, the current evidence base is dominated by preclinical studies and short-term human investigations, and direct evidence linking ketogenic dietary therapies to long-term cerebrovascular or cognitive outcomes remains limited. Conclusions: Ketogenic dietary therapies represent metabolically distinct dietary strategies with potential relevance for cerebrovascular and neuroprotective mechanisms. Nevertheless, human evidence remains heterogeneous and insufficient to support broad clinical recommendations. Future research should prioritize well-designed long-term human studies with clearly defined metabolic, cerebrovascular, and cognitive endpoints. Translational research frameworks may facilitate the evaluation of feasibility, safety, and implementation of ketogenic interventions in aging populations.

Population aging, the rising burden of chronic non-communicable diseases, and environmental degradation are increasingly recognized as interconnected global challenges, underscoring the need for integrated strategies that simultaneously promote human and planetary health. The Planetary Health Diet (PHD), originally proposed to address these challenges, has emerged as a promising dietary framework for supporting healthy aging. Although its health benefits are increasingly supported by epidemiological and clinical evidence, the biological mechanisms underlying these effects remain incompletely understood. This narrative review synthesizes evidence on the interplay among the PHD, the gut microbiome, and biological aging, with emphasis on microbiome-mediated pathways connecting sustainable nutrition with healthspan. Adherence to PHD-consistent dietary patterns is associated with greater microbial diversity and functional capacity, increased production of bioactive microbial metabolites, and more favorable intestinal barrier, immune, and metabolic profiles. These adaptations may modulate several hallmarks of aging and contribute to the preservation of physiological resilience. Evidence from prospective cohort studies, randomized controlled trials, and systematic reviews further indicates that dietary patterns consistent with the PHD are associated with lower risks of cardiometabolic diseases, frailty, cognitive decline, and premature mortality. By integrating findings from nutritional science, microbiome research, geroscience, and public health, this review positions the gut microbiome as an important, although not exclusive, biological interface through which sustainable dietary patterns may support healthspan while contributing to environmental sustainability.

Within the emerging field of nutritional neuroscience, omega-3 fatty acids are among the most extensively investigated dietary bioactive compounds with potential relevance to cognitive aging. As populations continue to age worldwide, identifying modifiable nutritional factors that support cognitive health has become an important public health priority. Docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA), obtained primarily from marine sources, are integral components of neuronal membranes and serve as precursors of specialized pro-resolving lipid mediators. This narrative review integrates concepts from nutritional neuroscience and geroscience to examine how dietary omega-3 fatty acids may influence biological pathways involved in age-related cognitive decline. Current evidence suggests that DHA and EPA affect multiple processes linked to brain aging, including neuroinflammation, synaptic plasticity, mitochondrial function, oxidative stress, cerebrovascular integrity, cellular senescence, and gut–brain axis signaling. These mechanisms overlap with several hallmarks of aging and may contribute to the maintenance of cognitive function during later life. Observational studies generally associate higher dietary intake or circulating omega-3 status with better cognitive performance and a lower risk of cognitive decline and dementia. Findings from randomized controlled trials are less consistent, although benefits appear more likely in individuals with low baseline omega-3 status, mild cognitive impairment, or increased biological vulnerability. Beyond their established anti-inflammatory effects, omega-3 fatty acids may influence multiple aging-related pathways, particularly inflammaging, vascular aging, and mitochondrial dysfunction. Although heterogeneity in study design, dosage, intervention timing, and participant characteristics precludes firm conclusions, viewing omega-3 fatty acids through a geroscience lens offers a useful framework for interpreting existing evidence and informing future research. Overall, omega-3 fatty acids represent a promising nutritional strategy for supporting cognitive health across the lifespan, warranting further investigation in well-characterized populations and precision nutrition approaches.