Background: An increasing number of studies suggest that diet plays an important role in regulating aging processes and modulates the development of the most important age-related diseases. Objective: The aim of this review is to provide an overview of the relationship between nutrition and critical age-associated diseases. Methods: A literature review was conducted to survey recent pre-clinical and clinical findings related to the role of nutritional factors in modulation of fundamental cellular and molecular mechanisms of aging and their role in prevention of the genesis of the diseases of aging. Results: Studies show that the development of cardiovascular and cerebrovascular diseases, neurodegenerative diseases, cognitive impairment and dementia can be slowed down or prevented by certain diets with anti-aging action. The protective effects of diets, at least in part, may be mediated by their beneficial macro- (protein, fat, carbohydrate) and micronutrient (vitamins, minerals) composition. Conclusions: Certain diets, such as the Mediterranean diet, may play a significant role in healthy aging by preventing the onset of certain diseases and by improving the aging process itself. This latter can be strengthened by incorporating fasting elements into the diet. As dietary recommendations change with age, this should be taken into consideration as well, when developing a diet tailored to the needs of elderly individuals. Future and ongoing clinical studies on complex anti-aging dietary interventions translating the results of preclinical investigations are expected to lead to novel nutritional guidelines for older adults in the near future.

Currently, an increasing amount of evidence supports the notion that vitamins C, D and E, carotenoids, and omega-3 fatty acids may protect against the progression of chronic respiratory diseases. Although chronic obstructive pulmonary disease (COPD) primarily affects the lung, it is often accompanied by extrapulmonary manifestations such as weight loss and malnutrition, skeletal muscle dysfunction, and an excess of harmful oxidants, which can lead to a decline in quality of life and possible death. Recently, the role of various vitamins, minerals, and antioxidants in mitigating the effects of environmental pollution and smoking has received significant attention. Therefore, this review evaluates the most relevant and up-to-date evidence on this topic. We conducted a literature review between 15 May 2018 and 15 May 2023, using the electronic database PubMed. Our search keywords included COPD, chronic obstructive pulmonary disease, FEV₁, supplementation: vitamin A, vitamin D, vitamin E, vitamin C, vitamin B, omega-3, minerals, antioxidants, specific nutrient supplementations, clinical trials, and randomized controlled trials (RCTs). We focused on studies that measured the serum levels of vitamins, as these are a more objective measure than patient self-reports. Our findings suggest that the role of appropriate dietary supplements needs to be reconsidered for individuals who are predisposed to or at risk of these conditions.

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.

Purpose: The goal of our review was to gather information on the most important community-acquired and hospital-acquired co-infections among coronavirus disease 2019 (COVID-19) patients, and to examine not only the effect of these co-infections on disease outcomes but also to identify the possible risk factors that predispose COVID-19 patients to co-infections. Methods: Medline (PubMed) and Google Scholar were searched for relevant articles published between January 1st, 2020, and September 31st, 2021, on the topic of co-infections among COVID-19 patients. Results: Among community-acquired and hospital-acquired co-infections, bacterial and fungal co-infections are equally frequent, followed by viral co-infections that affected a relatively smaller portion of patients. Overall, co-infections were more frequent in the hospital than at the community level. Risk factors for acquiring co-infections include male gender, longer length of hospital stay, presence of supportive treatment, such as ventilation, the admission to intensive care units, the administration of medications, such as steroids or antibiotics, and certain blood parameters, such as high C-reactive protein or lymphopenia. The presence of co-infections could aggravate the COVID-19 disease severity, prolong the healing time of patients, and lead to worse disease outcomes overall. Conclusion: Co-infections may increase the mortality of COVID-19 patients, especially in the hospital setting. Paying closer attention to hygiene, adhering to diagnostic and therapeutic protocols, implementing antimicrobial stewardship programs could decrease the occurrence of co-infections and lead to improved outcomes for COVID-19 patients.

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.

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.