Obesity has risen 38% since 2003, with a peak among young adults: these are the numbers at hand. The condition affects more than 6 million people, with 23.3 million Italians facing weight-related eating problems tied to overweight or obesity, according to the Italian Barometer Obesity Report 2025 from the Italian Barometer Diabetes Observatory (IBDO) Foundation, prepared in collaboration with Istat and other scientific partners.
Today, March 4th, World Obesity Day is observed. The condition is recognized as a chronic, progressive, and relapsing disease, included in the Essential Levels of Care (LEA) from October 1st, 2025 with the aim of facilitating access to treatment. However overweight, in its various forms, is accompanied by other important implications that deserve an integrated approach. Recent studies also indicate a crucial role for new contributing factors: the gut microbiome and pollution, among others.
A Complementary Set of Factors
Not a single cause, but multiple ones operating in synergy, compete and contribute to the development of obesity: individual responsibility such as physical inactivity and poor nutrition—for instance, regular consumption of fruits and vegetables has dropped from 94% in 1994 to about 78% in 2024—and environmental factors including pollution.
Obesity is not an isolated condition, but is linked to the development of more than 250 diseases, including type 2 diabetes, cardiovascular diseases, and cancers, responsible for around 57,000 deaths per year in Italy. The VII Italian Barometer Obesity Forum highlighted the need for systemic and multidisciplinary management to counter this “silent pandemic,” a trend rising especially among young adults and women. ISTAT’s generational analysis shows a much higher overweight rate at ages 20-24 among those born in the early 2000s (21.6%) than those born in the 1960s (13.4%), with an even more evident increase among women in the same age group—17.4% for those born 2000-2004 versus 9.0% for those born 1960-1964.
Sleep and Obesity: A Bidirectional Relationship
New evidence confirms a tight relationship between sleep disorders and obesity. Each condition can exacerbate the other through a complex interplay of behavioral, physiological, and hormonal mechanisms with strong implications for individual and public health.
Sleep deprivation and poor sleep quality contribute to energy imbalance by dysregulating appetite hormones such as leptin and ghrelin, increasing caloric intake, and reducing physical activity. Moreover, sleep disorders such as obstructive sleep apnea syndrome (OSAS), insomnia, and restless legs syndrome (RLS) are far more common among people with obesity.
Inflammation, autonomic dysregulation (i.e., faulty functioning of the autonomic nervous system that regulates involuntary functions like blood pressure, heart rate, and digestion), and neuroendocrine pathways play important roles in these relationships.
Sleep loss also amplifies components of metabolic syndrome, including insulin resistance and dyslipidemia, perpetuating further weight gain. Likewise, obesity-induced sleep disorders trigger pro-inflammatory states, vascular dysfunction, and sympathetic overactivity, worsening cardiometabolic risks. This is the finding of a systematic review by Italian researchers, published in Nutrition, Metabolism & Cardiovascular Diseases, underscoring the bidirectional link between obesity and sleep disorders and the need to integrate sleep assessment and management into obesity treatment strategies.
Addressing this relationship could help mitigate the progression of cardiometabolic comorbidities and improve overall health outcomes. The intertwined dynamics between obesity, sleep disorders, and mental health—mediated by inflammatory pathways, hormonal dysregulation, and neurobehavioral factors—once again underscore the need for integrated care with therapeutic approaches targeting physical, psychological, and sleep dimensions to improve health and quality of life for people living with obesity.
The Role of the Gut Microbiome
A study from India, published in Gut Microbes, analyzed metagenomic sequencing data of the gut microbiome to evaluate and understand the obesity-host microbiome relationship. It used 3,329 samples, including 1,494 from obese individuals and 1,835 controls, spanning 17 different countries, including data on 16S rRNA gene sequencing, a metagenomic technique that enables examination of the gut microbiome’s composition and its relation to obesity, and on whole metagenome sequencing.
In particular, fecal metagenomic data from diverse geographic regions were curated, profiled, and aggregated using a machine-learning approach to identify robust global signatures associated with obesity.
While microbial species and gut pathways were systematically integrated across the species’ genomic content to identify factors contributing to functional changes linked to obesity. The structure of the gut microbiome in obese individuals was assessed, noting a reproducible depletion of diversity in obese subjects compared with lean ones. The findings suggest that the loss of diversity in the gut of obese individuals may be responsible for perturbations in the healthy functional microbial repertoire; specifically, 25 highly predictive species and 37 pathway associations emerged as signatures of obesity, validated with markedly high accuracy (AUC: species 0.85 and pathways 0.80) using an independent validation dataset.
Thus, a reduction in short-chain fatty acid (SCFA) producers was observed, including several Alistipes species and Odoribacter splanchnicus, along with a depletion of promoters of gut barrier integrity such as Akkermansia muciniphila and Bifidobacterium longum in the guts of people with obesity. The data thus suggest that SCFA biosynthesis and purine/pyrimidine metabolism pathways are typical of the control group, whereas obese individuals show enrichment in amino acid biosynthesis, enzymatic cofactors, and peptidoglycan pathways.
Finally mapping the factors that contribute to important functional changes associated with obesity, researchers observed that these factors are dataset-specific as well as shared across datasets. In short, a comprehensive analysis of multiple datasets reveals the species that contribute specifically to functional changes and the coherent intestinal microbial models associated with obesity.
The Pollution Connection
The literature on the association between pollution, stress, and obesity is limited and a synthesis of knowledge on these three factors is not yet available. A systematic review of MEDLINE, Embase, and Web of Science Core Collection was conducted independently by multiple reviewers to identify studies addressing the effects of semi-volatile organic compounds, pesticides, preservatives, and heavy metals on psychosocial stress responses and adiposity in humans, animals, and cells.
Across the evidence, a positive association between pollution, stress, and obesity emerged, with an interdependent relationship: pollution stimulates the hypothalamic-pituitary-adrenal axis by activating glucocorticoid receptor signaling and transcription factors responsible for adipocyte differentiation, hyperphagia, and obesity.
Moreover, it was shown that endocrine disruptors also alter the peroxisome proliferator-activated receptor (PPAR) pathway—an entire class of chemicals, including various drugs and endogenous substances like fatty acids, that activate PPARs, which regulate the expression of genes involved in lipid and glucose metabolism, inflammation, and peroxisome biogenesis.
A dynamic that promotes adipocyte hyperplasia and hypertrophy, fueling obesity, though these associations may act independently and vary by sex, age, and type of pollutant. A common thread remains the hypothesis that pollution promotes stress, leading to obesity.
Sources
Figorilli M, Velluzzi F, Redolfi S. Obesity and sleep disorders: A bidirectional relationship. Nutrition, Metabolism and Cardiovascular Diseases, 2025, 35, 104014. DOI: https://doi.org/10.1016/j.numecd.2025.104014
Chanda D, De D. Meta-analysis reveals obesity associated gut microbial alteration patterns and reproducible contributors of functional shift. Gut Microbes, 2024, 16(1):2304900. DOI: 10.1080/19490976.2024.2304900
El Kouche S, Halvick S, Morel C et al. Pollution, stress response, and obesity: A systematic review. Obesity Reviews, 2025, 26(5):e13895. DOI: 10.1111/obr.13895
Abbonati a Karla Miller
