Associations of maternal lifestyle factors with inadequate pregnancy weight gain: findings from the baseline data of the LIMIT prospective cohort study.

BACKGROUND/OBJECTIVES: Gestational Weight Gain (GWG) impacts maternal and fetal health; deviations from optimal ranges pose health risks. Maternal lifestyle before and during pregnancy strongly influences GWG. This study explores factors linked to inadequate GWG, focusing on Mediterranean Diet (MD) adherence and specific food consumption. SUBJECTS/METHODS: 178 pregnant women were enrolled at Fondazione IRCCS Policlinico San Matteo (Pavia) during pre-hospital care before birth meeting inclusion/exclusion criteria. Sociodemographic data, pre-pregnancy BMI, GWG, MD adherence, physical activity (PA) levels, and smoking habits were retrospectively collected. Validated questionnaires adapted for the target group, assessed MD adherence and PA level. Participants were classified into adequate (AGWG) and inadequate GWG groups following IOM guidelines. RESULTS: Among 200 pregnant women (aged 30-36), 37.1% experienced low GWG and 24.1% excessive GWG. Our study revealed a significant association between inadequate GWG and educational level (P = 0.011); pre-pregnancy BMI (P = 0.005); MD adherence (P = 0.008), and daily average consumption of vegetables (P < 0.001). Our results also showed that a lower risk of EGWG vs. AGWG was associated with daily average consumption of vegetables (RRR = 0.279, P = 0.004), while a higher risk of EGWG vs. AGWG was associated with high daily meat product consumption (> 1.5 portions/day) (RRR = 7.83, P = 0.03). CONCLUSION: These findings emphasize the importance of promoting lifestyle changes before and during pregnancy to tackle the increasing incidence of inadequate GWG and improve the health outcomes of both mother and child.

Rethinking food policy framework to tackle childhood obesity in the Italian context.

Pediatric obesity has been described by the World Health Organization as 1 of the most serious public health challenges of the 21st century. Projections of increasing burdens of pediatric obesity and its related diseases on society highlight the need for urgent and substantial action. Many scientific and public debates about the prevention of childhood obesity are centered around simple dichotomies presenting a single-level solution. In contrast, efficient prevention programs should overcome these overly simplistic dichotomies and proceed in the early years of life within the family environment and the whole society, throughout one's lifetime. Food policies have the potential to counteract pediatric obesity by creating healthy food environments. However, the current food policies approach lacks monitoring indicators to assess short- and long-term impact, and is not well integrated into regional, national, and cross-cutting initiatives. Therefore, redesigning and rethinking food policy strategies and goals is an important opportunity to address childhood obesity, safeguard the planet, and contribute to economic and social prosperity.

Assessment of Epicardial Fat in Children: Its Role as a Cardiovascular Risk Factor and How It Is Influenced by Lifestyle Habits.

Epicardial adipose tissue (EAT) stands out as a distinctive repository of visceral fat, positioned in close anatomical and functional proximity to the heart. EAT has emerged as a distinctive reservoir of visceral fat, intricately interlinked with cardiovascular health, particularly within the domain of cardiovascular diseases (CVDs). The aim of our overview is to highlight the role of EAT as a marker for cardiovascular risk in children. We also explore the influence of unhealthy lifestyle habits as predisposing factors for the deposition of EAT. The literature data accentuate the consequential impact of lifestyle choices on EAT dynamics, with sedentary behavior and unwholesome dietary practices being contributory to a heightened cardiovascular risk. Lifestyle interventions with a multidisciplinary approach are therefore pivotal, involving a nutritionally balanced diet rich in polyunsaturated and monounsaturated fatty acids, regular engagement in aerobic exercise, and psychosocial support to effectively mitigate cardiovascular risks in children. Specific interventions, such as high-intensity intermittent training and circuit training, reveal favorable outcomes in diminishing the EAT volume and enhancing cardiometabolic health. Future clinical studies focusing on EAT in children are crucial for advancing our understanding and developing targeted strategies for cardiovascular risk management in this population.

Maternal Exposure to Endocrine-Disrupting Chemicals: Analysis of Their Impact on Infant Gut Microbiota Composition.

Endocrine disruptors (EDCs) are chemicals that interfere with the endocrine system. EDC exposure may contribute to the development of obesity, type 2 diabetes, and cardiovascular diseases by impacting the composition of an infant's gut microbiota during the first 1000 days of life. To explore the relationship between maternal urinary levels of Bisphenol-A and phthalates (UHPLC-MS/MS), and the composition of the infant gut microbiota (16S rDNA) at age 12 months (T3) and, retrospectively, at birth (T0), 1 month (T1), and 6 months (T2), stool samples from 20 infants breastfed at least once a day were analyzed. Metataxonomic bacteria relative abundances were correlated with EDC values. Based on median Bisphenol-A levels, infants were assigned to the over-exposed group (O, n = 8) and the low-exposed group (B, n = 12). The B-group exhibited higher gut colonization of the Ruminococcus torques group genus and the O-group showed higher abundances of Erysipelatoclostridium and Bifidobacterium breve. Additionally, infants were stratified as high-risk (HR, n = 12) or low-risk (LR, n = 8) exposure to phthalates, based on the presence of at least three phthalates with concentrations exceeding the cohort median values; no differences were observed in gut microbiota composition. A retrospective analysis of gut microbiota (T0-T2) revealed a disparity in ß-diversity between the O-group and the B-group. Considering T0-T3, the Linear Discriminant Effect Size indicated differences in certain microbes between the O-group vs. the B-group and the HR-group vs. the LR-group. Our findings support the potential role of microbial communities as biomarkers for high EDC exposure levels. Nevertheless, further investigations are required to deeply investigate this issue.

Could Celiac Disease and Overweight/Obesity Coexist in School-Aged Children and Adolescents? A Systematic Review.

Background: Celiac disease (CD) is a multifactorial, immune-mediated enteropathic disorder that may occur at any age with heterogeneous clinical presentation. In the last years, unusual manifestations have become very frequent, and currently, it is not so uncommon to diagnose CD in subjects with overweight or obesity, especially in adults; however, little is known in the pediatric population. This systematic review aims to evaluate the literature regarding the association between CD and overweight/obesity in school-age children. Methods: The Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines were followed. An electronic database search of articles published in the last 20 years in English was carried out in Web of Sciences, PubMed, and Medline. The quality of the included studies was assessed by using the STrengthening the Reporting of OBservational studies in Epidemiology statement. Results: Of the 1396 articles identified, 9 articles, investigating overweight/obesity in children/adolescents affected by CD or screening CD in children/adolescents with overweight/obesity, met the inclusion criteria. Overall, the results showed that the prevalence of overweight or obesity in school-age children (6-17 years) affected by CD ranged between 3.5% and 20%, highlighting that the coexistence of CD with overweight/obesity in children is not uncommon as previously thought. Conclusion: Although CD has been historically correlated with being underweight due to malabsorption, it should be evaluated also in children with overweight and obesity, especially those who have a familiar predisposition to other autoimmune diseases and/or manifest unusual symptoms of CD.

Breast and Formula Milk and Early Puberty Onset.

Nutrients have an enormous impact on many hormonal systems and aspects of health, and nutrition status is a crucial regulator of growth and pubertal development in children and adolescents. In this narrative review, we explore the connection between these feeding methods and the timing of puberty to provide a clearer understanding of how infant nutrition might contribute to the early development of puberty. Puberty is a key stage in the transition from childhood to adulthood and the timing of puberty represents a significant biological milestone of growth. Breast milk seems to have a pivotal role in puberty onset, mainly due to its dynamism, which shape indirectly the gut microbiota in early life, besides direct exposure of the baby to the milk microbiota through gut-breast axis. Concerning breast and formula milk and their effects on the onset of puberty, a protective role of the former occurs. As for the potential harmful effects of soy-based formulas and the isoflavones that they contain, the studies reported demonstrate conflicting opinions, underlining the need for further research on this topic. A healthy and well-nourished diet from the earliest stages of life has significant preventive potential for overall well-being, reducing the risk of many health problems later in life.

LIMIT: LIfestyle and Microbiome InTeraction Early Adiposity Rebound in Children, a Study Protocol.

Childhood obesity is a strong predictor of adult obesity with health and economic consequences for individuals and society. Adiposity rebound (AR) is a rise in the Body Mass Index occurring between 3 and 7 years. Early adiposity rebound (EAR) occurs at a median age of 2 years and predisposes to a later onset of obesity. Since obesity has been associated with intestinal dysbiosis, we hypothesize that EAR could be related to early microbiome changes due to maternal/lifestyle changes and environmental exposures, which can increase the unhealthy consequences of childhood obesity. LIMIT is a prospective cohort study that aims at identifying the longitudinal interplay between infant gut microbiome, infant/maternal lifestyle, and environmental variables, in children with EAR vs. AR. Methods. The study evaluated 272 mother-infant pairs, enrolled at an Italian neonatal unit, at different time points (T0, at delivery; T1, 1 month; T2, 6 months; T3, 12 months; T4, 24 months; T5, 36 months after birth). The variables that were collected include maternal/infant anthropometric measurements, lifestyle habits, maternal environmental endocrine disruptor exposure, as well as infant AR. The LIMIT results will provide the basis for early identification of those maternal and infant modifiable factors on which to act for an effective and personalized prevention of childhood obesity.

Crohn's Disease and Female Infertility: Can Nutrition Play a Supporting Role?

Crohn's disease (CD) is a chronic inflammatory disease (IBD) that can affect the entire gastrointestinal tract in a non-continuous mode. CD is generally diagnosed most commonly between 15 and 35 years of age and may affect female fertility. The role of diet in supporting wellbeing outcome and reproductive potential in women is well-known; however, no effective efforts have been made to improve women's awareness in CD. Our review aims to describe the burden of CD on women's fertility, reporting the most relevant nutrients that support reproductive function to ensure women diagnosed with IBD an adequate health-related quality of life.

Elongating RNA polymerase II and RNA:DNA hybrids hinder fork progression and gene expression at sites of head-on replication-transcription collisions.

Uncoordinated clashes between replication forks and transcription cause replication stress and genome instability, which are hallmarks of cancer and neurodegeneration. Here, we investigate the outcomes of head-on replication-transcription collisions, using as a model system budding yeast mutants for the helicase Sen1, the ortholog of human Senataxin. We found that RNA Polymerase II accumulates together with RNA:DNA hybrids at sites of head-on collisions. The replication fork and RNA Polymerase II are both arrested during the clash, leading to DNA damage and, in the long run, the inhibition of gene expression. The inactivation of RNA Polymerase II elongation factors, such as the HMG-like protein Spt2 and the DISF and PAF complexes, but not alterations in chromatin structure, allows replication fork progression through transcribed regions. Attenuation of RNA Polymerase II elongation rescues RNA:DNA hybrid accumulation and DNA damage sensitivity caused by the absence of Sen1, but not of RNase H proteins, suggesting that such enzymes counteract toxic RNA:DNA hybrids at different stages of the cell cycle with Sen1 mainly acting in replication. We suggest that the main obstacle to replication fork progression is the elongating RNA Polymerase II engaged in an R-loop, rather than RNA:DNA hybrids per se or hybrid-associated chromatin modifications.