The scale of that mortality burden helps explain why ESE has chosen to invest in a focused, small-cohort training programme rather than relying on general continuing medical education. Obesity is no longer viewed simply as a consequence of lifestyle choices; it is increasingly understood as a chronic, relapsing, multifactorial endocrine disease involving dysregulation of appetite pathways, adipose tissue function, insulin signalling and reproductive hormones. As the scientific understanding of obesity continues to evolve, endocrinologists play an essential role in its prevention, diagnosis and management. The new School has been developed to complement existing obesity education across Europe, with a specific and deliberate focus on obesity as an endocrine disease, an angle that distinguishes it from broader weight-management courses aimed at general practitioners or public health specialists.

The three-day, in-person programme will cover both the clinical and mechanistic aspects of obesity, bringing together leading experts from across Europe to explore the latest developments in this rapidly evolving field. According to Gregory Kaltsas, chair of the ESE Education Committee, the format is built around interactive learning, case-based discussions and networking opportunities, so that participants gain valuable scientific knowledge while building relationships that support future collaboration and research. The curriculum reads like a survey of the field’s current frontiers. Topics include the genetics of obesity, adipose tissue biology and function, food noise, weight regain, treatments, new frontiers in the field, and the intersections between obesity and endocrinology across the life course, including puberty, menopause and polyendocrine metabolic ovarian syndrome.

Several of those topics deserve closer attention, because they map directly onto the most active areas of obesity science today. The genetics of obesity, for instance, has been transformed by large-scale genome-wide association studies that have identified hundreds of genetic variants influencing body mass index, many of which act through the central nervous system’s regulation of hunger and satiety. Understanding monogenic and polygenic forms of obesity allows clinicians to stratify patients, anticipate disease trajectories and, in a growing number of cases, select targeted therapies. Adipose tissue biology, meanwhile, has shifted from viewing fat as a passive energy store to recognising it as a dynamic endocrine organ that secretes hormones such as leptin and adiponectin, modulates inflammation and determines metabolic health outcomes in ways that vary dramatically between individuals of the same body weight.

The inclusion of food noise and weight regain on the syllabus reflects two of the most discussed clinical phenomena of the current treatment era. Food noise, a term popularised by patients describing persistent intrusive thoughts about food, has become a focal point for research into how brain reward and hunger circuits drive eating behaviour, and how modern pharmacotherapies appear to quieten it. Weight regain, conversely, remains the central challenge of long-term obesity management: physiological adaptations, including reduced resting energy expenditure and elevated appetite signalling, conspire to restore lost weight after almost every intervention, whether dietary, surgical or pharmacological. Teaching early-career clinicians why regain happens, and how emerging combination therapies might counteract it, is precisely the kind of mechanistic training the School intends to provide.

The target audience is equally specific. The School is aimed at Fellows and early-career clinicians with experience in the obesity field who are seeking to further specialise in this area of endocrinology. Participation is application-based and limited to a maximum of 25 fellows, a deliberately small number intended to create a highly interactive learning environment in which every attendee can engage directly with faculty. All successful applicants will also be invited to present a clinical case report during dedicated programme sessions, an element that transforms passive attendance into active scholarly contribution and gives young clinicians experience in presenting complex, real-world patient scenarios to senior experts.

The scientific calibre of the faculty is a central part of the offering. The Scientific Programme Committee comprises eight of Europe’s leading endocrinologists with a specialism in obesity: Blandine Gatta Cherifi (France), Karine Clément (France), Daniela Cota (France), Maeve Durkan (Ireland), Melania Manco (Italy), Uberto Pagotto (Italy), Kristina Saravinosvka (Serbia) and Liesbeth van Rossum (Netherlands). The group spans several of the continent’s most productive obesity research centres, and its multinational composition signals ESE’s intention to make the School a genuinely European platform rather than a national or single-centre initiative. For applicants, the prospect of three days of close contact with this level of expertise is likely to be the strongest draw.

Daniela Cota, speaking as a representative of the Scientific Programme Committee, framed the launch as an investment in the specialty’s future. She described obesity as one of the most pressing health challenges of our time and emphasised that endocrinologists have a vital role to play in improving outcomes for people living with the disease. Through the launch of the School, she said, ESE is supporting talented early-career clinicians and researchers to develop the expertise, networks and confidence needed to lead progress in the field. She added that the new School reflects ESE’s commitment to advancing endocrine science and clinical care while ensuring members have access to high-quality education in areas of growing importance, and expressed enthusiasm about welcoming applications for the inaugural event and supporting a new generation of obesity specialists.

The practical arrangements are designed to lower barriers to participation. Successful applicants will receive access to the full educational programme, accommodation and catering during the event, while a limited number of meeting grants will be available for eligible ESE members from low- and middle-income countries, a provision aimed at ensuring the School draws talent from across the entire WHO European Region rather than only its wealthier western half. The venue, Sabàtic Gavà Mar in Barcelona, a Tribute Portfolio Hotel, is conveniently located near Barcelona Airport, enabling participation from attendees across Europe and beyond with minimal travel friction, an apparently small logistical detail that matters considerably for a three-day intensive course drawing an international cohort.

The application window is already open and closes on 1 October 2026, giving prospective fellows a defined period to prepare their submissions. Applicants should submit a covering letter outlining their interest in attending, together with a curriculum vitae, a publication list and an optional supporting letter from a supervisor. Further information and application details are available on the ESE event website. For a field in which new drug classes, genetic insights and neuroscientific models of appetite are reshaping clinical practice at unprecedented speed, the arrival of a dedicated European training school for obesity endocrinology marks a significant institutional commitment, and the 25 fellows selected for the Barcelona inaugural will be among the first clinicians trained specifically to lead that transformation.

Subject of Research: A new European training school for early-career specialists in obesity endocrinology

Article Title: European Society of Endocrinology launches new Obesity and Endocrinology School for 2027

Article References: European Society of Endocrinology launches new Obesity and Endocrinology School for 2027. (n.d.). Original publication

Image Credits: AI Generated

DOI: Not provided

Keywords: obesity, endocrinology, European Society of Endocrinology, medical education, Barcelona, adipose tissue, weight regain, food noise, genetics of obesity, early-career clinicians, fellowship, WHO European Region

The past few decades have witnessed astonishing progress in deciphering obesity’s genetic landscape. Since the seminal discovery of leptin in the mid-1990s, researchers have identified more than 85 monogenic forms of obesity. These monogenic variants typically manifest as early-onset obesity and are frequently accompanied by disruptions in appetite regulation and neurodevelopmental abnormalities, underscoring their syndromic nature. Unlike polygenic obesity, where multiple genes exert subtle effects, monogenic obesity arises from mutations in a single gene, leading to profound physiological consequences.

Genome-wide association studies (GWAS) have propelled our insights even further by pinpointing over a thousand loci linked to variations in body weight. These loci predominantly lie within genes active in the central nervous system, indicating that the brain’s regulation of energy balance and feeding behavior is central to obesity. This extensive polygenic architecture highlights that obesity is far from a single-gene disorder; it is a mosaic of genetic variations cumulatively influencing susceptibility.

Translating these genetic discoveries into therapeutic interventions marks a paradigm shift in obesity management. One striking example is the development of melanocortin 4 receptor (MC4R) agonists. MC4R plays a critical role in appetite and energy expenditure regulation, and mutations in this receptor are among the most common genetic causes of monogenic obesity. Targeted pharmacological activation of MC4R has demonstrated remarkable efficacy in rebound weight loss and reduction of associated metabolic complications, showcasing the potential of genetically informed therapies.

Beyond pharmacology, advances in genomics enable a more nuanced stratification of obese patients based on their underlying genetic etiology. This stratification lays the groundwork for precision medicine, where treatments are tailored not only according to phenotype but also the specific genetic drivers. Such personalized approaches bear the promise of improving therapeutic outcomes and minimizing adverse effects, which remain significant hurdles in the current one-size-fits-all paradigm.

While leptin deficiency and MC4R mutations provide clear examples of monogenic contributions, the vast majority of obesity cases fall into the polygenic category. These involve hundreds to thousands of genetic variants, each contributing a small effect size but collectively exerting substantial influence over lifetime obesity risk. The challenge lies in integrating these polygenic risk scores into clinical practice, as they require sophisticated computational models and population-specific validation.

Neurodevelopmental phenotypes associated with monogenic obesity emphasize the intricate interplay between brain development and metabolic regulation. This complexity suggests that early-life interventions may be critical for preventing or mitigating obesity in genetically susceptible individuals. Understanding how genetic mutations disrupt neurocircuitry that controls appetite and satiety could unlock novel preventative strategies beyond conventional lifestyle modifications.

Environmental factors undoubtedly interact with genetic predispositions to shape obesity risk, highlighting the importance of epigenetics. Epigenetic modifications can modulate gene expression without altering the DNA sequence and are influenced by diet, stress, and other exposures. Investigating how epigenetic mechanisms intersect with genetic variants could reveal critical windows for intervention and potential reversible targets.

Public health strategies stand to benefit from these genetic insights by incorporating genetic screening and counseling into obesity prevention programs. Early identification of high-risk individuals allows for personalized lifestyle recommendations and closer clinical monitoring. However, ethical considerations such as genetic privacy and potential stigmatization must be thoughtfully addressed when implementing such strategies on a population scale.

Indubitably, the multifactorial nature of obesity demands a multidisciplinary research approach. Collaborative efforts spanning molecular genetics, neuroscience, endocrinology, and computational biology are essential to capture the complete picture. In particular, leveraging multi-omics data—integrating genomics, transcriptomics, proteomics, and metabolomics—can provide an unprecedented resolution of obesity’s molecular underpinnings.

Another promising avenue lies in the realm of gene editing technologies, such as CRISPR-Cas9, which theoretically enable correction of pathogenic mutations causing monogenic obesity. While clinical applications remain in their infancy due to technical and ethical challenges, these tools represent a future horizon where genetic cures may become feasible.

The complex genetic architecture of obesity also provides fertile ground for drug discovery beyond MC4R agonists. Identifying novel targets within adipose tissue biology, energy homeostasis pathways, or gut-brain signaling circuits may yield new classes of therapeutics. Importantly, these drugs can be designed with genetic backgrounds in mind, thereby maximizing efficacy and safety profiles.

As precision medicine advances, integrating genetic data into electronic health records and clinical decision support systems will facilitate personalized treatment algorithms. This integration demands robust bioinformatics infrastructures alongside clinician education to interpret and apply genetic findings effectively, ensuring that benefits reach patients at the bedside.

In summation, the genetics of obesity is drastically reshaping our conceptualization and treatment of this pervasive metabolic disorder. With over a billion individuals affected worldwide, incorporating genetic knowledge into prevention and therapy offers a beacon of hope to stem the tide of obesity-related morbidity. Future research endeavors promise to unravel deeper layers of complexity and drive the next generation of interventions designed to improve health outcomes globally.

Subject of Research: The genetics of obesity focusing on monogenic, oligogenic, and polygenic contributions and the impact of genetic discoveries on prevention and therapy.

Article Title: The genetics of obesity: aetiology, prevention and therapy.

Article References:
Bonnefond, A., Bruner, W.S., Grant, S.F.A. et al. The genetics of obesity: aetiology, prevention and therapy. Nat Metab (2026). https://doi.org/10.1038/s42255-026-01497-w

Image Credits: AI Generated

DOI: https://doi.org/10.1038/s42255-026-01497-w