The Sick Adipocyte Theory: The Forces of Clustering at Glance

Abstract

The concept and repercussions of Obesity have evolved alongside Humankind. First seen as an advantageous trait in the beginning of time, it s now a double edged sword definition that shows how slowly genometabolic traits are acquired and how quickly can environmental factors turn it around. Being obese is not only a matter of Body Mass Index (BMI) and adiposity, its influence stretches out to include type 2 Diabetes Mellitus (T2DM), Psychological disorders like depression, anxiety disorders, and other eating disorders, Osteoarticular problems, Metabolic Syndrome, Cardiovascular Diseases (CVD) like hypertension, stroke, and myocardial infarction, Neurological disorders, Cancer, and even Immunity-related issues, such as low grade inflammation (Must, 1999; Oster, 2000; Thompson, 2001; Marchesini, 2003; Adami, 2003; Niskanen, 2004; Panagiotakos, 2005). Obesity has been rising slowly yet steadily ever since the Industrial revolution and its pace has increased since the dawn of the 20th Century. Even though nutritional disorders have plagued Man, it was common to see that undernutrition and malnourishment were the higher numbers around the globe. Yet, the tables were turned when Gardner & Halweil published in 2000 that the number of excess-weight patients surpassed the number of the underweight population, welcoming Humanity to the supersized phase of the land of milk and honey (O Dea, 1992). In 2006, the World Health Organization reported that by 2005 1.6 billion above 15 years of age would be overweight and at least 400 million would be obese, while it is predicted to reach 2.3 billion of overweight and over 700 million of obese adults by the year 2015 (World Health Organization [WHO], 2006). The figures published by Kelly et al, 2008 darken the scope, predicting that by 2030 1.12 billion individuals will be obese and 2.16 million will be overweight. There are many factors that have influenced the increasing prevalence of obesity worldwide, and have influenced the scientific community to coin the term obesogenic environment (Egger & Swinbum, 1997) as the external factors that act as “second hit” triggers in the