For years, there has been a public debate about dietary sugar intake and its role in the development of obesity and NCDs, including type 2 diabetes (T2D), cardiovascular diseases (CVDs), and cancer. There are several definitions of dietary sugars available; they include “added sugars”, which are all sugars and syrups that are added to foods during processing and preparation, “free sugars” which according to the definition of the World Health Organization (WHO) comprise all mono- and disaccharides that are added to foods by the manufacturer, cook or the consumer as well as the sugars that are naturally present in honey, syrups, and fruit juices. The definition “total sugars” includes all sugars that naturally occur in food as well as added sugars. These definitions naturally include all monosaccharides (e.g., glucose, fructose, and galactose) and all disaccharides (e.g., sucrose, lactose, and maltose). Since these definitions are often mixed up, the review will refer exactly to the definitions used in the original works to avoid confusion.
The role of dietary sugars in the development of obesity has been investigated in various meta-analyses, which deliver the highest quality of scientific evidence. Te Morenga and colleagues on behalf of the WHO investigated the role of free sugars at the onset of obesity by performing a systematic review and meta-analyses including randomized controlled trials as well as prospective cohort studies, which concluded that free sugars are a crucial determinant for body weight gain. A high intake of free sugars is associated with an excess calorie intake, which if not compensated by energy expenditure will lead to an increase of body fatness. Since the isocaloric exchange of free sugars with other carbohydrates was not associated with weight changes, the authors concluded that this effect is mediated by changes in energy intake. These results were confirmed by subsequent analyses of independent researchers. Fattore et al. performed a systematic review and meta-analyses in 2017 that showed that free sugars had no effect on body weight as long as they were isocalorically exchanged with other carbohydrates. Therefore, through the highest scientific evidence of human studies, it can be concluded that the consumption of free sugars will only result in overweight and obesity if more calories in the form of free sugars are consumed than expended. Free sugars per se do not favor body weight gain as shown by isocaloric exchange with other carbohydrates.
In beverages, sucrose can be replaced by artificial sweeteners, resulting in reduced energy content, whereas in solid foods, it is very difficult to reduce the amount of sucrose without changing technical properties and taste. Besides its sweetness, sucrose is important for bulk and texture as well as flavor formation of, e.g., bakery products. It reduces the water activity in foods resulting in increased shelf-life and is used for yeast fermentation. Currently, there is no other sweetener that can duplicate all or many of the functional properties of sucrose. Technical research has indicated that sucrose cannot simply be replaced by a single nutrient, but a mixture of nutrients or compounds must be used to replace the functional attitudes and sweetness of sucrose. Taken together, sucrose cannot easily be replaced by other nutrients in solid foods to reduce calorie content without affecting functional properties. If sucrose is replaced by other carbohydrates, the taste will diminish while the caloric value will not change; however, the replacement may have a different effect on blood glucose levels. If replaced by fat, it can be assumed that the calorie content of solid foods will increase.
Most of the available data on the effect of sugars in the development of T2D is available from observational studies. Since T2D is a disease that develops over years, it is not possible to investigate the impact of sugars on the long-term development of T2D in intervention studies. In 2010, the European Food Safety Agency (EFSA) stated that the available scientific data is insufficient for setting an upper level for the intake of added sugars based on their effect on T2D. Subsequently, Hauner and colleagues investigated the role of various carbohydrates on behalf of the German Nutrition Society (DGE). In line with the results of EFSA, they concluded that the association between the total intake of all mono- and disaccharides, including glucose and fructose, and the risk of T2D is considered to be insufficient. Added to that and because of the inconsistency of the results, the evidence regarding the lack of an association between sucrose intake and the risk of T2D is viewed as probable. In 2015, the British Scientific Advisory Committee on Nutrition (SACN) also stated that there is no association of daily intake of all dietary sugars and T2D due to limited evidence. In line with these results, a meta-analysis of prospective cohort studies concluded that total sugar and fructose cannot be associated with the onset of T2D and interestingly sucrose was associated with a decreased risk of T2D. All in all, current data does not support the theory that dietary sugars support the development of T2D. Therefore, the assumption that dietary sugars alone will cause T2D is scientifically not evaluated and wrong; however, obesity as a result of an unhealthy lifestyle is strongly related with the incidence of T2D.
Interestingly, a systematic review and meta-analysis of Xi and colleagues concluded that the increased intake of sugar-sweetened fruit juice was associated with the incidence of T2D, whereas an intake of 100% fruit juice was not. It is noteworthy, that in the previous systematic review and meta-analysis by Imamura and colleagues, ‘SSBs’ were defined as any sweetened beverages, including sugar-sweetened fruit juice, whereas ‘fruit juice’ was defined as 100% fruit juice, or fruit juice assessed separately from fruit drinks.
Added sugars as well as other dietary sugars are not associated with CVDs and that the current data is insufficient to set an upper level. Current scientific evidence from human intervention studies indicates that dietary sugars per se do not cause CVDs, but high sugar consumption, which exceeds energy expenditure, can cause body weight gain and obesity due to excessive calorie intake. It is well known that obesity is a major risk factor for CVDs and therefore, nutritional recommendations to prevent CVDs should focus on tackling obesity and reducing calorie intake rather than focusing on the reduced intake of a single nutrient.
The WCRF recommends keeping a healthy body weight balance by increasing physical activity and reducing the amount of fast food. These recommendations clearly point to a healthier lifestyle in order to reduce the risk of cancer by reducing body weight. The role of body weight in the development of cancer is further supported by a systematic review and meta-analysis, which showed that an increase in BMI by 5 kg/m. increases the risk of various types of cancer in men and women. Overall, there is very little evidence that dietary sugars are associated with different types of cancer. To reduce the risk of cancer, a healthy lifestyle with a moderate body weight is essential.
Current scientific evidence does not support the conclusion that dietary sugars themselves are detrimental to human health and the cause of obesity as well as NCDs. Data from human studies clearly shows that it is the excess amount of calories, also consumed in form of dietary sugars, that promotes obesity and with that favors NCDs. For sucrose, further research is needed in order to evaluate the relevance of its molecular composition, especially in comparison with other macronutrients.
Source: Prinz, P. The role of dietary sugars in health: molecular composition or just calories? European Journal of Clinical Nutrition volume 73, pages1216–1223 (2019)