Obesity has recently emerged as a major global health problem. According to World Health Organization (WHO) estimates, approximately 1.6 billion adults worldwide were overweight (BMI ≥ 25 kg/m2) and at least 400 million were obese (BMI ≥ 30 kg/m2) in 2005, numbers which are expected to reach 2.3 billion and 700 million respectively, by 2015. In the United States, the percentage of overweight and obese adults increased markedly from 47% and 15% in 1976-1980 to over 66% and 33% in 2005-2006, with the greatest proportion of increase seen among Non-Hispanic black and Mexican-American women 1, 2. The implications of excess body weight are far reaching. Epidemiologic studies indicate that overweight and obesity are important risk factors for of type 2 diabetes (T2DM), cardiovascular disease (CVD), cancer and premature death 3. In the US, health care expenditures attributable to overweight and obesity are estimated to be $147 billion or 9.1% of total health care costs per year4. Such excess costs could have serious repercussions for resource-poor countries, which must manage dual burdens of chronic and infectious disease.
In the setting of a pandemic of obesity and related chronic diseases, the American Heart Association recently released a scientific statement recommending reductions in added sugar intake to no more than 100-150 kcal per day for most Americans5. The statement identified sugar sweetened beverages (SSB) as the primary source of added sugars in the American diet6. While it has long been suspected that SSBs contribute at least in part to the obesity epidemic, only in recent years have large epidemiologic studies been able to substantiate the relationship between SSB consumption and long-term weight gain, T2DM and cardiovascular risk. It is thought that SSB’s contribute to weight gain due to their high added sugar content, low satiety and potential incomplete compensation for total energy leading to increased energy intake7, 8. In addition, because of their high amounts of rapidly absorbable carbohydrates such as various forms of sugar and high-fructose corn syrup (HFCS), and large quantities consumed, SSB’s may increase T2DM and cardiovascular risk, independent of obesity as a contributor to a high dietary glycemic load (GL) leading to inflammation, insulin resistance, and impaired ß-cell function 9. Fructose from any sugar or HFCS may also increase blood pressure, and promote accumulation of visceral adiposity, dyslipidemia and ectopic fat deposition due to increased hepatic de novo lipogenesis10. Here, we review temporal patterns in SSB consumption, and clinically relevant effects on obesity, T2DM and cardiovascular disease risk, emphasizing potential underlying biological mechanisms, clinical implications and consideration of methodological issues inherent in the literature.