This article describes the clinical case of a patient with multiple thyroid nodules who showed significant improvement after discontinuing the continuous use of perfumes and cosmetics with synthetic fragrances. The work also provides a brief review of the literature on the harmful effects of volatile chemical compounds present in perfumes, which can act as endocrine disruptors and contribute to thyroid dysfunction. The case reinforces the importance of considering environmental exposures as a potentially reversible factor in thyroid alterations. Natural fragrances, like synthetic ones, can also cause fragrance-related health issues and act as endocrine-disrupting chemicals (EDCs). Many people assume that “organic” or “natural” scents are safer, but research shows that natural essential oils also contain volatile organic compounds (VOCs) that can oxidize and form harmful byproducts, especially when exposed to air and ozone. For example, limonene, a common component of citrus-based essential oils, can react with ozone to generate formaldehyde and acetaldehyde, both of which are harmful to human health. Additionally, some natural fragrance compounds such as linalool, geraniol, and eugenol are known allergens and can act as potential endocrine disruptors. Therefore, even products labeled as “natural” or “organic” may still pose risks. These findings have been confirmed by several scientific studies, including research by Dr. Anne Steinemann, who has extensively analyzed the chemical emissions and health impacts of fragranced consumer products. Analytical methods such as GC-MS (Gas Chromatography-Mass Spectrometry) and LC-MS (Liquid Chromatography-Mass Spectrometry) are commonly used to detect VOCs and EDCs in fragrances.

Chronic diseases such as type 2 diabetes (T2DM) arise from complex interactions among genetic, behavioral, and environmental factors. While polygenic risk scores (PRS) have been widely adopted to quantify inherited risk, conventional approaches often aggregate genetic effects into a single score, limiting insight into the underlying biology of disease susceptibility. To address this, we present a platform that integrates partitioned polygenic risk scores (pPGS) —which reflect distinct physiological domains such as β-cell function, insulin processing, adipose tissue biology, and hepatic metabolism — with longitudinal lifestyle data and environmental context.

At the core of this approach is the OneHealth Knowledge Base, a structured repository of directional relationships between lifestyle factors (e.g., nutrients, foods, physical activity patterns, social behaviors) and specific health outcomes. These relationships were extracted from over 40 million scientific articles in PubMed and PMC using AI methods enhanced with manual curation. The knowledge base is being expanded to include relationships between lifestyle factors and molecular targets involved in disease development.

These relationships are operationalized through a digital healthware platform that includes: (1) assessments of individual-level behaviors and exposures; (2) linkage to community-level determinants of health using public datasets such as the American Community Survey (ACS), NHANES, and the U.S. Bureau of Labor Statistics; and (3) integration with genomic data via pPGS.

This presentation will describe the methodological framework used to develop and validate the partitioned scores, the annotation and inference pipeline behind the knowledge base, and the design of digital tools for capturing lifestyle behavior in free-living individuals. We will illustrate how the integration of pPGS with lifestyle data and curated evidence can be used to generate mechanistically-informed hypotheses, stratify risk, and guide the design of personalized interventions. Implications for research, clinical utility, and public health implementation will also be discussed.

The discovery of the ubiquitin-26S proteasome pathway fundamentally transformed our understanding of intracellular protein degradation. While this system remains central to proteostasis, it is now evident that the 20S core proteasome also functions autonomously, independently of ubiquitin and ATP. Given that nearly half of all cellular proteasomes exist as free 20S complexes, this mode of degradation is far from rare—yet its mechanisms and biological significance are only beginning to emerge.

In this talk, I will present our recent findings that illuminate the distinct roles of the 20S proteasome. Through systematic substrate profiling, we identified endogenous targets enriched in RNA- and DNA-binding proteins with intrinsically disordered regions, many localized to the nucleus and stress granules [1]. We also discovered a new class of modulators, which we term Catalytic Core Regulators (CCRs), that selectively tune 20S proteasomal activity [2,3]. Extending these insights beyond the cell, we characterized the circulating 20S proteasome in blood [4]. This uncapped complex displays unique post-translational modifications, enhanced caspase-like activity, and enrichment in immunoproteasome subunits—hallmarks of adaptation to extracellular conditions. Together, our studies redefine the 20S proteasome as a versatile and autonomous degradation system, essential for safeguarding proteostasis across both intracellular and extracellular environments, with broad implications for stress adaptation, immune function, and disease.

Bile acids are increasingly recognized as critical mediators of host-microbiome interactions, influencing a wide range of physiological processes including glucose and lipid metabolism, inflammation, and cardiovascular function. Beyond their classical role in dietary fat emulsification, bile acids act as signaling molecules through receptors such as FXR and TGR5, linking gut microbial activity to systemic health. While the microbial conversion of primary to secondary bile acids—primarily via bile salt hydrolase (BSH) and 7α-dehydroxylase pathways—is well established, the dynamic responsiveness of this system to acute dietary changes, particularly fasting, remains incompletely understood.

In this study, we investigated how a five-day 250 kcal vegetable juice-only fasting intervention affects gut microbiota composition and secondary bile acid metabolism in humans. Thirty-six healthy adults underwent supervised fasting, with fecal and plasma samples collected immediately before and after the intervention. To assess shifts in key microbial taxa associated with bile acid metabolism and gut barrier integrity, we performed quantitative PCR (qPCR) targeting Akkermansia muciniphila, Bacteroides ovatus, Bacteroides fragilis, and Prevotella copri. These taxa were selected based on their known involvement in mucin degradation, bile acid modification, and metabolic disease associations. However, qPCR analysis revealed no statistically significant changes in their relative abundance following fasting. Despite the absence of significant taxonomic shifts, previous studies suggest that microbial functions can adapt independently of community structure. To explore this further, shotgun metagenomic sequencing is currently underway to identify potential changes in the functional capacity of the microbiome, particularly in genes involved in bile acid metabolism such as the bile acid-inducible (bai) operon and BSH-related pathways. These preliminary findings highlight the complexity and potential disconnect between microbial composition and function, emphasizing the importance of multi-omic approaches in microbiome research. Functional changes in bile acid metabolism during short-term fasting may have important implications for metabolic flexibility and gut-liver axis signaling, even in the absence of major taxonomic shifts. Ultimately, this work contributes to a more nuanced understanding of how acute nutritional interventions influence host-microbiome dynamics and opens new avenues for targeting bile acid pathways in the context of metabolic and cardiovascular health.

Food systems worldwide are responsible for a large share of anthropogenic environmental impacts and face growing scrutiny due to their significant environmental, social, and economic impacts. As the global population continues to expand, it exerts greater pressure on existing food systems. The unsustainability of these systems, exacerbated by food waste, overconsumption and unsustainable diets, poses a major challenge to achieving long-term ecological and societal well-being. Through case studies developed in my recent research, this presentation not only describes the main aspects that make the current food systems unsustainable but also provides insights into how research is evolving to reduce the unsustainability of this system. In particular, the reduction of impact through different animal and human diets, as well as the potentiality to recycle biowaste, are discussed based on recent findings. The emerging topic of cultured meat is also addressed, highlighting the potential consequences of using this novel food. Systemic methods used to estimate the environmental impact of food systems, such as LCA, are introduced to present the related results. Mitigation scenarios based on specific analyses are presented. This presentation aims to delve into a crucial topic by providing an overview of, on one hand, the main challenges on the horizon, and on the other, the most important and emerging solutions currently being addressed within international research.