Background: Women are typically diagnosed with estrogen receptor-positive breast cancer around the postmenopausal period when declining estrogen levels initiate changes in lipid profiles. Aromatase inhibitors (AI) are used to prevent the progression of cancer; however, a further reduction in estrogen levels may have detrimental effects on lipid levels, which was our working hypothesis. Methods: Our meta-analysis was conducted on the lipid profiles of postmenopausal breast cancer patients at baseline and at different treatment time points. Results: We identified 15 studies, including 1708 patients. Studies using anastrozole (ANA), exemestane (EXE), letrozole (LET), and tamoxifen (TMX) were involved. Subgroup analyses revealed that 3- and 12-month administrations of LET and EXE lead to negative changes in lipid profiles that tend to alter the lipid profile undesirably, unlike ANA and TMX. Conclusions: Our results suggest that, despite statistically significant results, EXE and LET may not be sufficient to cause severe dyslipidemia in patients without cardiovascular comorbidities according to the AHA/ACC Guideline on the Management of Blood Cholesterol. However, the results may raise the question of monitoring the effects of AIs in patients, especially those with pre-existing cardiovascular risk factors such as dyslipidemia.

Post-harvest fungicides are frequently used on citrus peels to reduce post-harvest fungal contamination during the storage and transport of products. Despite these positive effects, fungicides can pose health risks to consumers. The aim of our study was to perform a genotoxicological risk assessment of imazalil, pyrimethanil, thiabendazole and their mixtures used as post-harvest treatments. A Salmonella mutagenicity Ames test and comet assay were performed to detect reverse mutation and assess DNA damage. Base-pair, frameshift mutations and metabolic activity were analyzed using the Ames test. In the comet assay, lymphocytes were treated with fungicides for 4 and 24 h. Thiabendazole was found to induce both frameshift and base-pair mutations in the Ames test despite the mutagenicity of both imzalil and pyrimethanil (p < 0.05). DNA-strand breaks were observed in lymphocytes, mainly with dimethyl-sulfoxide solvent fungicides (p < 0.05). The long-term exposure and consumption of fruits and vegetables treated with fungicides can increase the risks of developing genotoxic tumors. Our findings raise new questions about the health risks of fungicides and their mixtures to consumers. Further investigations are essential to explore the genotoxicological effects of fungicides on citrus peels.

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.

Background: Rheumatoid arthritis (RA) is chronically persistent synovitis and systemic inflammation. Although multiple contributors are detected, only one is pivotal in the neonatal period: the negative selection of autoimmune naïve T-cells by the autoimmune regulator (AIRE) transcriptional factor. Methods: Single-nucleotide polymorphisms (SNPs) in the DNA-binding site of AIRE may determine its function and expression. We intended to analyse site-specific allelic polymorphisms in two exon (rs878081 and rs1055311) and three intron (rs1003853, rs2075876, and rs1003854) loci with an RA risk. Our analytical case-control study analysed 270 RA patients and 322 control subjects in five different genetic models using quantitative real-time PCR (qPCR) with TaqMan^® assays. Results: Statistically significant differences were found between the odds of allelic polymorphisms in the loci of rs878081, rs1003854, and rs1003853 among the controls and RA patients, and the disease activity seemed to be significantly associated with the genotypic subgroups of rs878081 and rs1055311. Our in silico analysis supported this, suggesting that allele-specific alterations in the binding affinity of transcriptional factor families might determine RA activity. Conclusion: Our findings highlight the involvement of neonatal self-tolerance in RA pathogenesis, providing novel insights into disease development and paving the way for an analysis of further site-specific genetic polymorphisms in AIRE to expand the intervention time for RA.