The obesity epidemics in ESRD: from wasting to waist?

During the last six decades, from the World War II years on, the phenotype of human beings has changed profoundly. The dominant slim, pale and light phenotype of the 1920s has gradually been overthrown by the heavy, large and ponderous phenotype of obese people. Obesity is rampant in the USA (http://www.cdc.gov/nccdphp/dnpa/ obesity/trend/maps/, accessed on 20th July 2008) and, even though to a lesser degree, most European countries share the same epochal evolution [1]. Type 2 diabetes and cardiovascular diseases are the two most important noncommunicable disease outcomes of obesity. Abdominal obesity is strongly associated, and at least in part in a causal manner, with hypertension, dyslipidaemia and impaired insulin resistance [2]. Well beyond these complications, neoplasia [3], greater exposure to drugs of various sort, sterility [4], asthma [5], non-alcoholic liver disease [6] and osteoarthritis [7] are all much concerning sequelae of this epidemics. The risk of disease and disability attributable to overweight and obesity starts early, just when the upper limit of the ideal body mass index (BMI) (21–23 kg/m2) is trespassed and rises linearly at progressively higher BMI levels [8,9]. The burden of disease attributable to excess BMI among adults in the USA is enormous. Obesity at age 40 years reduced life expectancy by ∼7 years in women and by ∼6 years in men in the Framingham cohort [10]. In Europe, more than 1 million deaths and ∼12 million lifeyears of ill health (disability adjusted life-years—DALYs) were counted in 2000 [9].