The role of sugar-sweetened beverages in the global epidemics of obesity and chronic diseases

Abstract

Sugar-sweetened beverages (SSBs) are a major source of added sugars in the diet. A robust body of evidence has linked habitual intake of SSBs with weight gain and a higher risk (compared with infrequent SSB consumption) of type 2 diabetes mellitus, cardiovascular diseases and some cancers, which makes these beverages a clear target for policy and regulatory actions. This Review provides an update on the evidence linking SSBs to obesity, cardiometabolic outcomes and related cancers, as well as methods to grade the strength of nutritional research. We discuss potential biological mechanisms by which constituent sugars can contribute to these outcomes. We also consider global trends in intake, alternative beverages (including artificially-sweetened beverages) and policy strategies targeting SSBs that have been implemented in different settings. Strong evidence from cohort studies on clinical outcomes and clinical trials assessing cardiometabolic risk factors supports an aetiological role of SSBs in relation to weight gain and cardiometabolic diseases. Many populations show high levels of SSB consumption and in low-income and middle-income countries, increased consumption patterns are associated with urbanization and economic growth. As such, more intensified policy efforts are needed to reduce intake of SSBs and the global burden of obesity and chronic diseases.

Fig. 1. Global trends in sugar-sweetened beverage intake by sex.

Mean intake of sugar-sweetened beverages (SSBs) (grams of SSB per day) from 1990 to 2015 in seven world super-regions, that is, grouping of world regions that exhibit similar cause-of-death patterns. These are: Asia, comprising east and Southeast Asia, former Soviet Union countries (FSU), western high-income countries (HIC), Latin America and Caribbean countries (LAC), Middle East and north Africa (MENA), south Asia (SAARC), and sub-Saharan Africa (SSA). Data are shown separately for men (part a) and women (part b). For reference, 237 g of SSB is equivalent to 8 fl oz (237 ml) of SSB and 355 g of SSB is equivalent to 12 fl oz (355 ml) of SSB. Data are obtained from: Global Dietary Database.

Fig. 2. Global intake of sugar-sweetened beverages in 1990 and 2015.

Mean intake of sugar-sweetened beverages (SSBs) (grams of SSB per day) in 1990 (part a) and 2015 (part b). The colour of individual countries corresponds to SSB consumption level, with lower intakes shown in green (0–200 g per day) and higher intakes shown in red (500–600 g per day). Countries with no data are shown in white. Data are for men and women combined. For reference, 237 grams of SSB is equivalent to 8 fl oz (237 ml) of SSB and 355 grams of SSB is equivalent to 12 fl oz (355 ml) of SSB. Data are obtained from: Global Dietary Database.

Fig. 3. Biological mechanisms for sugar-sweetened beverage intake and development of obesity, cardiometabolic risk and related chronic diseases.

Biological mechanisms linking intake of sugar-sweetened beverages (SSBs) to the development of obesity, intermediate cardiometabolic risk factors (such as non-alcoholic fatty liver disease, hypertension, insulin resistance, inflammation and dyslipidaemia) and related chronic diseases (the metabolic syndrome, type 2 diabetes mellitus (T2DM), cardiovascular disease and cancer). Mechanisms that promote weight gain and obesity include: an incomplete compensatory reduction in food intake in response to liquid calories provided by SSBs; hyperinsulinaemia induced by rapid absorption of glucose; and potential activation of the dopaminergic reward system in the brain. Obesity increases cardiometabolic risk and is associated with the development of related chronic diseases. Elevated risk of these outcomes also occurs independently of weight gain through the development of risk factors precipitated by adverse glycaemic effects and fructose metabolism in the liver. Excess fructose ingestion promotes uric acid production, hepatic de novo lipogenesis, accumulation of visceral adipose tissue (VAT) and ectopic lipid deposition, and can lead to the development of gout and non-alcoholic fatty liver disease. HFCS, high-fructose corn syrup. Adapted from ref., CC BY 4.0 (https://creativecommons.org/licences/by/4.0/).