Genetics of Obesity Syndromes
Philip L. Beales is Professor of Medical and Molecular Genetics and Honorary Consultant in Clinical Genetics at the Great Ormond Street Children’s Hospital in London. I. Sadaf Farooqi is Researcher in the Metabolic Research Laboratories at the Institute of Metabolic Science at Addenbrooke’s Hospital in Cambridge. Stephen O’Rahilly is Professor in the Metabolic Research Laboratories at the Institute of Metabolic Science at Addenbrooke’s Hospital in Cambridge. Together they edited, Genetics of Obesity Syndromes, which looks at both the molecular and clinical features of the obesity syndromes, providing hard-core information for researchers and practical guidance for clinicans caring for obese patients. In the excerpt below we learn why obesity is increasingly a problem and how it is measured.
Never before in history has there been such an abundance of energy-rich, highly processed foodstuffs. However, the price of progress is beginning to be felt among more Westernized populations with seemingly inexorable rises in the prevalence of obesity, diabetes, and cardiovascular disease. This so-called nutrition transition combined with increasingly sedentary lifestyles is promoting an obesogenic environment, which according to the World Health Organization (WHO) is now the greatest risk factor for ill health worldwide (Drewnowski and Popkin 1997). Latest estimates predict that 400 million of the world’s population is now obese (World Health Organisation 2006). In North America, the rates of overweight and obese children and adolescents have tripled over the last 30 years. In the United States alone, one-third of the population is obese; and this rate is climbing annually. Many countries in Europe are closely following behind, and even less developed nations are witnessing significant increases in the prevalence of obesity. This epidemic is by no means confined to adlts, with an increasing proportion of children and adolescents becoming morbidly obese. Concomitant medical problems such as type 2 diabetes mellitus, traditionally the domain of adults, are increasingly recognized in children (Fagot-Campagna 2000). Is is this cocktail of relative inactivity and calorie availability that appears to be unmasking our underlying genetic susceptibility to weight gain – presumably an advantage for many of our “hunter-gatherer” ancestors (Neel 1962).
Obesity refers to an excess accumulation of adipose tissues. Exactly what constitutes excessive is questionable; and furthermore, how this shall be measured is hotly debated. Adiposity is a continous trait and is not easily measure; therefore, a surrogate estimate of obesity now tends toward excess body weight. This is usually presented as the weight adjusted for height or the body mass index (BMI), calculated by weight in kilograms divided by height in meters squared.
In 1981, Garrow first proposed a grading system based on BMI. He defined obesity grades I, II, and III by BMI classes of 30-39.9 kg/m^2 and 40kg/m^2 or above, for both men and women. A value of 25 was considered the upper limit of a normal or healthy BMI in North Americans and Europeans. A WHO expert committee defined overweight as a BMI of 25 and greater and obesity is described with a BMI of 40 or more.
The BMI, although easy to calcuate, can be misleading if considered our of context. For example, a short male muscle builder can have the same BMI as an obese tall woman.