Manuel Bicho

Background/Aim: Traditional Portuguese cuisine is a key component of the country’s cultural identity. Understanding how traditional Portuguese dishes align with, or diverge from, the principles of a balanced and sustainable diet is essential for promoting healthy eating habits while preserving cultural heritage. The aims of this study were: (a) to evaluate and compare the nutritional composition of traditional Portuguese recipes from different regions; and (b) to assess the adequacy of complete regional menus in relation to recommendations for a balanced and healthy meal. Methodology: A pilot study was conducted analysing 60 traditional Portuguese recipes from three regions of mainland Portugal (North, Centre, and South). Twenty recipes per region were evaluated, including six first courses, eight main courses, and six desserts. Nutritional composition was determined per 100 g, and regional differences were analysed using one-way ANOVA with Tukey’s post hoc test (p < 0.05). Six complete menus were also constructed and assessed against reference values for energy and nutrient intake. Results: Significant differences were observed in the energy (p = 0.02) and sodium (p = 0.03) content of first-course dishes, particularly between the Northern region and the other regions. The Central region showed higher mean dietary fibre values. No statistically significant regional differences were identified for main courses or desserts. Menu analysis revealed that most traditional menu combinations exceeded recommended energy values and showed imbalances in macronutrient distribution, notably excessive saturated fat and insufficient dietary fiber. Conclusions: Traditional Portuguese first-course dishes display relevant regional nutritional differences. Overall, complete traditional menus frequently fall short of current nutritional recommendations, emphasizing the need for culturally sensitive adaptations that maintain culinary heritage while supporting public health goals, namely by lowering saturated fat and sodium content and enhancing dietary fibre levels.

Heart failure (HF) is frequently associated with iron deficiency and anemia, negatively impacting patient outcomes. This study aimed to investigate the contribution of genetic variation in iron metabolism-related genes to biochemical and hematological phenotypes in HF. An HF population of 182 patients with functional iron deficiency (ID) and anemia was stratified by sex and heart failure subtype, including HF with reduced ejection fraction (HFrEF) and HF with non-reduced ejection fraction (HFnrEF). Genetic variants in HFE (rs1799945), SLC40A1 (rs1439816, rs2304704), and TMPRSS6 (rs855791) were evaluated. Variants in HFE and SLC40A1 were associated with differences in serum iron, ferritin, transferrin saturation, hemoglobin, and RDW. The phenotypic impact of these variants was modulated by sex and heart failure subtype, highlighting the influence of iron availability, inflammatory burden, and erythropoietic demand. In contrast, no significant associations were observed for the TMPRSS6 variant. In conclusion, genetic variation in key regulators of iron metabolism contributes to the heterogeneity of iron-related biochemical and hematological phenotypes in HF. These findings emphasize the interplay between genetic background, sex, and heart failure physiology and support the relevance of personalized approaches to iron assessment and management in heart failure.

Hepatitis C virus (HCV) infection is a global health concern, chronically affecting over 71 million people. It primarily targets the liver but also causes systemic complications through inflammation, oxidative stress, and metabolic dysregulation. HCV is a highly variable RNA virus with six major genotypes that are mainly transmitted via blood. Often asymptomatic, the infection progresses silently to chronic hepatitis C (CHC), which can lead to fibrosis, cirrhosis, and hepatocellular carcinoma (HCC). Direct-acting antivirals (DAAs) have revolutionized treatment, achieving cure rates above 95%, improving liver function, reversing fibrosis, and normalizing metabolism. HCV disrupts iron metabolism by suppressing hepcidin, causing iron overload and oxidative stress. It also alters lipid metabolism, inducing steatosis, and affects glucose metabolism, contributing to insulin resistance and type 2 diabetes. DAAs improve these metabolic outcomes. HCV promotes oxidative stress via viral proteins, damaging liver cells and DNA and triggering inflammation and fibrogenesis. Even post-cure, oxidative stress and iron overload may continue to drive disease progression. Genetic and epigenetic factors influence fibrosis progression and HCC risk. Despite a sustained virologic response (SVR), patients with advanced liver damage remain at risk for HCC and metabolic diseases, highlighting the need for continued monitoring and personalized post-treatment care.

Chronic hepatitis C (CHC) is linked to iron overload, which significantly correlates with liver fibrosis. This study aimed to assess whether genetic polymorphisms related to iron metabolism are associated with fibrosis severity, predict improvement in fibrosis after HCV clearance with direct-acting antivirals (DAAs) and influence iron-related metabolic markers before treatment. A total of 329 CHC patients were included, 134 of whom received DAAs therapy. Liver fibrosis was assessed using transient elastography (FibroScan), and biochemical parameters were measured using standard methods. Eighteen genetic polymorphisms within five iron metabolism-related genes were analyzed using PCR-RFLP, endpoint genotyping, or next-generation sequencing (NGS). Before DAA treatment, patients with severe fibrosis showed higher levels of serum iron (Fe), total iron-binding capacity (TIBC), and ferritin (Ft). SLC40A1 rs1439816_GG was associated with an increased risk of severe fibrosis compared with GC or CC genotypes. SLC40A1 rs11568351_GC genotype was linked to a higher likelihood of remaining cirrhotic after HCV clearance. Elevated iron parameters were observed in carriers HFE C282Y_CY, TF IVS 11 G>A, and BMP2 570 A>T. Overall, polymorphisms in iron metabolism genes may influence both the severity of liver fibrosis prior to treatment, its regression after DAA therapy and the regulation of iron metabolism in CHC patients.

Human papillomavirus (HPV) infection plays a crucial role in cervical carcinogenesis. The link between the autonomic nervous system and tumor biology is increasingly being recognized. Understanding how neural signaling pathways interact with HPV oncogenesis could open new avenues for therapeutic intervention. We aim to study the contribution of the autonomic nervous system-related genes to the HPV-associated cervical lesions. A population of 140 HPV-infected women presenting cervical lesions was compared to a control population. Genes/variants under study were: BDNF/rs6265, NTRK2/rs2289656, NGF/rs6330, SLC6A4/5-HTT variable number tandem repeats intron 2, HTR2A/rs6313, ADRBR2/rs1042713, and CHRNA5/rs16969968. Samples were genotyped using polymerase chain reaction (PCR), PCR-restriction fragment length polymorphism, and endpoint genotyping. Statistical analysis revealed a genetic contribution for SCL6A4, ADRB2, and CHRNA5. SCL6A4 showed statistically significant association in the codominant (p=0.003) and dominant models (p=0.024, odds ratio [OR] = 2.301). ADRB2 showed statistically significant association in the codominant (p<0.001), dominant (p=0.024, OR = 4.728), recessive (p<0.001, OR = 4.856), and allelic models (p<0.001, OR = 4.091), while CHRNA5 showed statistically significant association in the dominant model (p=0.030, OR = 0.529). We conclude that there is a genetic contribution of the adrenergic (ADRB2), cholinergic (CHRNA5), and serotonergic (SLC6A4) systems to cervical lesions associated with HPV infections.

Retinal neurodevelopment, vascularization, homeostasis, and stress response are influenced by factors such as nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), tyrosine hydroxylase (TH), and erythropoietin (EPO). As retinopathy of prematurity (ROP) is a neurovascular retinal disease, this study analyzed the contributions of NGF (rs6330), BDNF (rs7934165), TH (rs10770141), and EPO (rs507392) genetic functional polymorphisms to the modulation of hematological and biochemical parameters of the first week of life and their association with ROP development. A multicenter cohort of 396 preterm infants (gestational age < 32 weeks or birth weight < 1500 g) was genotyped using MicroChip DNA and iPlex MassARRAY^® platform. Multivariate regression followed univariate assessment of ROP risk factors. NGF (GG) genotype was associated with a higher ROP risk (OR = 1.79), which increased further (OR = 2.38) when epistatic interactions with TH (allele C) and BDNF (allele G) were present. Significant circulating biomarker differences, including bilirubin, erythrocytes, monocytes, neutrophils, lymphocytes, and platelet markers, were found between ROP and non-ROP groups, with variations depending on the polymorphism. These findings suggest that NGF (rs6330) and its interactions with related genes contribute to ROP risk, providing valuable insights into the genetic and biological mechanisms underlying the disease and identifying potential predictive biomarkers.

Background/Objectives: Retinopathy of prematurity (ROP) is a leading cause of vision impairment in preterm infants, with its pathogenesis linked to oxygen exposure. Red blood cell (RBC) transfusions, commonly performed in neonatal intensive care units (NICUs), reduce fetal hemoglobin (HbF) fraction, altering oxygen dynamics and potentially contributing to ROP. We aimed to investigate the relationship between RBC transfusions, HbF percentage, and ROP, evaluating HbF as a potential predictive biomarker. Methods: A multicenter, prospective study was conducted across eight Portuguese NICUs, involving infants born at p < 0.05. Results: Eighty-two infants (mean GA: 28.1 ± 2.1 weeks, birth weight: 1055.8 ± 258.3 g) were included. Among them, 29 (35.4%) presented ROP and 4 (4.9%) required treatment. Infants with ROP had more RBC transfusions and lower HbF percentages than those without ROP (p < 0.05). Lower HbF was associated with more RBC transfusions (p < 0.001). Kaplan–Meier survival curves showed a higher ROP risk in infants with reduced HbF (p < 0.05). Conclusions: Low HbF percentage in the first four weeks of life may increase ROP risk in preterm infants. HbF could serve as a biomarker for ROP prediction. Interventions preserving HbF may reduce ROP risk. Further studies are needed to validate HbF as a biomarker and refine prevention strategies.

Background/Aim: Subfertility is characterized by a decrease in reproductive efficiency, which can result in delayed pregnancy, and affects one in six individuals during their lifetime. The present narrative review aims to evaluate the contribution of precision nutrition to changes in fertility in subfertile couples. Methods: The literature review was carried out through bibliographic research in the PubMed, Scopus, SciELO and Google Scholar databases. The following search criteria were applied: (1) original articles and narrative, systematic or meta-analytic reviews, and (2) the individual or combined use of the following keywords: “genetic variation”, “nutrigenetics”, “precision nutrition”, “couple’s subfertility”, and “couple’s infertility”. A preliminary reading of all the articles was carried out, and only those that best fit the themes and subthemes of the narrative review were selected. Results: Scientific evidence suggests that adherence to a healthy diet that follows the Mediterranean pattern is associated with increased fertility in women and improved semen quality in men, better metabolic health and reduced levels of inflammation and oxidative stress, as well as maintaining a healthy body weight. The integration of different tools, such as nutrigenetics, predictive biochemical analyses, intestinal microbiota tests and clinical nutrition software, used in precision nutrition interventions can contribute to providing information on how diet and genetics interact and how they can influence fertility. Conclusions: The adoption of a multidisciplinary and precision approach allows the design of dietary and lifestyle recommendations adapted to the specific characteristics and needs of couples with subfertility, thus optimizing reproductive health outcomes and achieving successful conception.

This systematic review aims to explore the diagnostic criteria, epidemiology, etiology, and prognosis of Human Papillomavirus (HPV) infection in lung cancer. This PRISMA-guided review searched the PubMed^® and Embase^TM databases for “lung cancer AND HPV” on 10 June 2023, filtering human subject papers. A total of 97 studies encompassing 9098 patients worldwide, revealing varied HPV infection rates in lung cancer, ranging from 0% to 69%, were analyzed. While HPV16/18 was predominant in some regions, its association with lung cancer remained inconclusive due to conflicting findings. Studies from Asia reported lower HPV infection rates compared to Western populations. Some studies suggested a limited role of HPV in lung carcinogenesis, particularly in non-smokers. However, intriguing associations were noted, including HPV’s potential role in lung adenocarcinoma and squamous cell carcinoma. Discrepancies in HPV detection methods and sample sources highlight the need for further research with standardized methodologies to elucidate HPV’s role in lung carcinogenesis and its clinical implications. Overall, this systematic review offers insights into HPV’s role in lung cancer epidemiology and clinical characteristics. Despite inconclusive evidence, intriguing associations between HPV and lung adenocarcinoma and squamous cell carcinoma have emerged. Further research with standardized methodologies and larger cohorts is needed for clarity.

Background/Objectives: Retinopathy of prematurity (ROP) is a retinal neovascular disease affecting preterm infants. Identifying risk factors for its development and progression is critical for effective screening and prevention. This study aimed to analyze the incidence of ROP and identify key risk factors for its development and progression. Methods: We conducted a prospective, observational cohort study on 455 neonates (gestational age [GA] < 32 weeks or birth weight < 1500 g) across eight Portuguese NICUs. Results: ROP incidence was 37.8%, with 4.6% requiring treatment. Multivariate analysis identified low GA and the number of red blood cell (RBC) transfusions as significant factors for ROP development and progression. After adjusting for these variables, platelet transfusions, high maximum fraction of inspired oxygen (FiO₂) in the second week, and surfactant use remained significantly associated with ROP development, while early and late sepsis, maternal chronic hypertension, and delayed enteral nutrition were associated with progression to ROP requiring treatment. Conclusions: These findings underscore the importance of addressing low GAs and adult RBC transfusions in ROP risk management and suggest that maximum FiO₂, platelet transfusions, and sepsis also play crucial roles. Larger studies are needed to validate these results and explore preventive interventions, particularly regarding the impact of multiple adult RBC transfusions on fetal hemoglobin percentages.