In 2020, an estimated 2.6 billion people worldwide were overweight or obese (BMI ≥25kg/m²), and it is predicted that this could reach over 4 billion people by 2035. Obesity is the result of complex interactions between genetic, socio-economic and cultural influences. Lifestyle changes that lead to a decrease in energy intake and an increase in energy expenditure would help combat this development, In addition environmental factors such as the use of chemicals in agriculture (e.g. pesticides), food preservation and packaging (e.g. plasticisers) and other areas of daily life could play an increasingly important role in this context.

Obesity is closely associated with (metabolic) comorbidities such as type 2 diabetes, metabolic dysfunction-associated fatty liver disease, cardiovascular diseases and certain types of cancer. Furthermore, abnormalities in lipid metabolism are very common in obese individuals. However, the individual risk of developing cardiometabolic diseases is not solely determined by fat mass. There are people who remain metabolically healthy despite being obese, while individuals with normal weight or very low subcutaneous fat mass may develop typical obesity-related diseases.

Recent advances in research have made it clear that obesity is a heterogeneous condition, and studies in recent years have focused particularly on the subtyping of obesity. The main focus has been on metabolically healthy obesity, i.e. a transient state in which people with obesity do not have an immediate metabolic disorder, but many of them develop a metabolically unhealthy state if obesity persists. In this context, advances in research and technology, particularly in the fields of genomics, metabolomics and precision medicine, may help to further unravel the intricacies of obesity.

To date, body mass index (BMI) is often used as a measure to assess the risk of comorbidities. However, due to differences between sexes, age and other factors, there are large inter-individual differences in estimating body fat content based on BMI data. In addition, BMI only takes into account total body fat, not body fat distribution. It is now known that the metabolic risk associated with obesity is largely dependent on the distribution of body fat, with visceral adipose tissue playing a particularly important role. 

Studies have shown that genetic and epigenetic alterations, changes in the immune system, dysbiosis of the gut microbiome and dysregulation of adipokines play a crucial role in mediating the pathogenic link between visceral adipose tissue and comorbidities. Therefore, quantification of visceral adipose tissue is important for assessing the risk of obesity-related complications and for timely targeted treatment. Currently, a number of anthropometric indicators have been proposed for the determination of visceral adipose tissue, such as the visceral adiposity index (VAI), waist circumference, and the lipid accumulation product. The VAI, for example, is a simple gender-specific algorithm calculated from waist circumference, BMI, triglycerides and high-density lipoprotein cholesterol and has recently proven to be an indicator of adipose tissue distribution and function, and thus indirectly expresses cardiometabolic risk. 

First and foremost, lifestyle changes should be considered in the treatment of obesity. A high quality hypocaloric diet combined with at least 150 minutes of moderate physical activity per week is recommended for weight loss. However, to achieve weight loss at the individual level, it is important to create a personalized lifestyle program in which weight loss goals are realistically chosen, reviewed and set for the long term. This should take into account the patient's motivation, personal weight loss goals, eating habits, dietary preferences, weight-related complications and previous attempts of lifestyle change. If behavioral interventions are not sufficiently effective in achieving individual weight loss, obesity pharmacotherapy with currently available medications for long-term weight control in adults in conjunction with lifestyle modification may be considered.

At the population level, the first aim is to stop a rise in obesity prevalence and the accumulation of more and more fat mass in already obese persons. To make it very clear the ultimate success would be to stop the development of overweight and obesity during childhood and adolescence, and by this setting grounds for a normal body weight in adulthood.

Up to now, social and environmental challenges, lack of physical exercise and a wide range of easily affordable, energy-rich foods continue to diminish hopes of getting control or better eliminating the global obesity epidemic. The key to effectively combating the disease lies in significant and sustained weight loss and its the long-term maintenance. To date, strategies to prevent and treat obesity - both at an individual and population level - have not been successful in the long term. Lifestyle and behavioral interventions aimed at reducing caloric intake and increasing energy expenditure have limited efficacy because complex and persistent hormonal, metabolic, and neurochemical adaptations prevent weight loss and promote weight regain. Through refined pathophysiological phenotyping and classification of individuals according to their obesity subtypes, tailored interventions could be developed to address the associated risks and optimize therapeutic outcomes.