The objectives of this study were to explore the relation between body mass index (BMI) and prevalence of diabetes mellitus, hypertension and dyslipidaemia; examine BMI distributions among patients with these conditions; and compare results from two national surveys. The Study to Help Improve Early evaluation and management of risk factors Leading to Diabetes (SHIELD) 2004 screening questionnaire (mailed survey) and the National Health and Nutrition Examination Surveys (NHANES) 1999-2002 (interview, clinical and laboratory data) were conducted in nationally representative samples>or=18 years old. Responses were received from 127,420 of 200,000 households (64%, representing 211,097 adults) for SHIELD, and 4257 participants for NHANES. Prevalence of diabetes mellitus, hypertension and dyslipidaemia was estimated within BMI categories, as was distribution of BMI levels among individuals with these diseases. Mean BMI was 27.8 kg/m2 for SHIELD and 27.9 kg/m2 for NHANES. Increased BMI was associated with increased prevalence of diabetes mellitus, hypertension and dyslipidaemia in both studies (por=25 kg/m2. Estimated prevalence of diabetes mellitus and hypertension was similar in both studies, while dyslipidaemia was substantially higher in NHANES than SHIELD. In both studies, prevalence of diabetes mellitus, hypertension and dyslipidaemia occurred across all ranges of BMI, but increased with higher BMI. However, not all overweight or obese patients had these metabolic diseases and not all with these conditions were overweight or obese. Except for dyslipidaemia prevalence, SHIELD was comparable with NHANES. Consumer panel surveys may be an alternative method to collect data on the relationship of BMI and metabolic diseases.

When caloric intake exceeds caloric expenditure, the positive caloric balance and storage of energy in adipose tissue often causes adipocyte hypertrophy and visceral adipose tissue accumulation. These pathogenic anatomic abnormalities may incite metabolic and immune responses that promote Type 2 diabetes mellitus, hypertension and dyslipidemia. These are the most common metabolic diseases managed by clinicians and are all major cardiovascular disease risk factors. 'Disease' is traditionally characterized as anatomic and physiologic abnormalities of an organ or organ system that contributes to adverse health consequences. Using this definition, pathogenic adipose tissue is no less a disease than diseases of other body organs. This review describes the consequences of pathogenic fat cell hypertrophy and visceral adiposity, emphasizing the mechanistic contributions of genetic and environmental predispositions, adipogenesis, fat storage, free fatty acid metabolism, adipocyte factors and inflammation. Appreciating the full pathogenic potential of adipose tissue requires an integrated perspective, recognizing the importance of 'cross-talk' and interactions between adipose tissue and other body systems. Thus, the adverse metabolic consequences that accompany fat cell hypertrophy and visceral adiposity are best viewed as a pathologic partnership between the pathogenic potential adipose tissue and the inherited or acquired limitations and/or impairments of other body organs. A better understanding of the physiological and pathological interplay of pathogenic adipose tissue with other organs and organ systems may assist in developing better strategies in treating metabolic disease and reducing cardiovascular disease risk.

The ongoing obesity epidemic represents a global public health crisis that contributes to poor health outcomes, reduced quality of life, and >2.8 million deaths each year. Obesity is relapsing, progressive, and heterogeneous. It is considered a chronic disease by the World Obesity Federation (WOF) and a chronic condition by the World Heart Federation (WHF). People living with overweight/obesity are at greater risk for cardiovascular (CV) morbidity and mortality. Increased adiposity (body fat), particularly visceral/abdominal fat, is linked to CV risk and CV disease (CVD) via multiple direct and indirect pathophysiological mechanisms. The development of CVD is driven, in part, by obesity-related metabolic, endocrinologic, immunologic, structural, humoral, haemodynamic, and functional alterations. The complex multifaceted nature of these mechanisms can be challenging to understand and address in clinical practice. People living with obesity and CVD often have concurrent chronic physical or psychological disorders (multimorbidity) requiring multidisciplinary care pathways and polypharmacy. Evidence indicates that intentional weight loss (particularly when substantial) lowers CVD risk among people with overweight/obesity. Long-term weight loss and maintenance require ongoing commitment from both the individual and those responsible for their care. This position paper, developed by the WOF and the WHF, aims to improve understanding of the direct and indirect links between overweight/obesity and CVD, the key controversies in this area and evidence relating to cardiometabolic outcomes with available weight management options. Finally, an action plan for clinicians provides recommendations to help in identifying and addressing the risks of obesity-related CVD (recognizing resource and support variances between countries).