Consumption of added sugar is associated with development and/or prevalence of fatty liver, dyslipidemia, insulin resistance, hyperuricemia, cardiovascular disease and type 2 diabetes, and many of these associations are independent of body weight gain or total energy intake. Stanhope KL. Sugar consumption, metabolic disease and obesity: The state of the controversy. Crit Rev Clin Lab Sci. 2016;53(1):52-67. doi:10.3109/10408363.2015.1084990. Available at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4822166/
We revisit an old hypothesis that sugar,particularly excessive fructose intake, has a critical role in the epidemic of cardiorenal disease. We also present evidence that the unique ability of fructose to induce an increase in uric acid may be a major mechanism by which fructose can cause cardiorenal disease.Finally, we suggest that high intakes of fructose in African Americans may explain their greater predisposition to develop cardiorenal disease. Johnson RJ, Segal MS, Sautin Y. Potential role of sugar (fructose) in the epidemic of hypertension,obesity and the metabolic syndrome, diabetes, kidney disease, and cardiovascular disease. Am J Clin Nutr. 2007;86:899–906. Available at https://watermark.silverchair.com/znu01007000899.pdf
A growing body of evidence suggests that sugars might have various adverse health effects. High intake of sugars may be related with an increased risk of several disorders including dental caries, obesity, cardiovascular disease, diabetes, gout, fatty liver disease, some cancers, components of the metabolic syndrome, and hyperactivity. Heidari-Beni M., Kelishadi R. (2016) The Role of Dietary Sugars and Sweeteners in Metabolic Disorders and Diabetes. In: Merillon JM., Ramawat K. (eds) Sweeteners. Reference Series in Phytochemistry. Springer, Cham. https://doi.org/10.1007/978-3-319-26478-3_31-1. Available at https://link.springer.com/referenceworkentry/10.1007%2F978-3-319-26478-3_31-1
High sugar consumption and sedentary lifestyle are associated with increased obesity prevalence. Siervo, M., Montagnese, C., Mathers, J., Soroka, K., Stephan, B., & Wells, J. (2014). Sugar consumption and global prevalence of obesity and hypertension: An ecological analysis. Public Health Nutrition, 17(3), 587-596. doi:10.1017/S1368980013000141. Available at https://www.cambridge.org/core/journals/public-health-nutrition/article/sugar-consumption-and-global-prevalence-of-obesity-and-hypertension-an-ecological-analysis/59A063A3E178E83F55174800788A397B
Sugar can induce metabolic syndrome in mice independently of its sweet properties. Andres-Hernando A, Kuwabara M, Orlicky DJ et al. Sugar causes obesity and metabolic syndrome in mice independently of sweet taste. American Journal of Physiology-Endocrinology and Metabolism. August 2020;319(2):E276-E290. https://doi.org/10.1152/ajpendo.00529.2019. Available at https://journals.physiology.org/doi/abs/10.1152/ajpendo.00529.2019?journalCode=ajpendo
Epidemiological studies support liquid added sugars, such as soft drinks, as carrying greater risk for development of metabolic syndrome compared with solid sugar. Some studies suggest that fruit juice may also confer relatively higher risk for weight gain and insulin resistance compared with natural fruits. Experimental evidence suggests this may be due to differences in how fructose is metabolized. Fructose induces metabolic disease by reducing the energy levels in liver cells, mediated by the concentration of fructose to which the cells are exposed. The concentration relates to the quantity and speed at which fructose is ingested, absorbed, and metabolized. Although reduced intake of added sugars (sucrose and high-fructose corn syrup) remains a general recommendation, there is evidence that sugary soft drinks may provide greater health risks relative to sugar-containing foods. Available at https://www.practiceupdate.com/content/the-form-of-sugar-intake-and-the-risk-for-metabolic-syndrome/83490
This paper will present evidence for the link between glucose, diabetes, obesity, metabolic syndrome and incident HF. Horwich TB, Fonarow GC. Glucose, obesity, metabolic syndrome, and diabetes relevance to incidence of heart failure. J Am Coll Cardiol. 2010;55(4):283-293. doi:10.1016/j.jacc.2009.07.029. Available at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2834416/
The consumption of soft drinks can increase the prevalence of NAFLD independently of metabolic syndrome. During regular soft drinks consumption, fat accumulates in the liver by the primary effect of fructose which increases lipogenesis, and in the case of diet soft drinks, by the additional contribution of aspartame sweetener and caramel colorant which are rich in advanced glycation end products that potentially increase insulin resistance and inflammation. Nseir W, Nassar F, Assy N. Soft drinks consumption and nonalcoholic fatty liver disease. World J Gastroenterol. 2010;16(21):2579-2588. doi:10.3748/wjg.v16.i21.2579. Available at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2880768/
This review has examined how negative emotion can exacerbate sugar overconsumption, and vice versa. If negative emotions are so prevalent in our children, and sugar intake so common, its consumption may be considered a threat to the emotional stability of our race (see reviews on mental health in children and adolescents. More importantly, reduction of sugar overconsumption may be capable of significantly reducing the prevalence of negative emotion in a vast number of individuals around the world. Jacques A, Chaaya N, Beecher K, Ali SA, Belmer A, Bartlett S. The impact of sugar consumption on stress driven, emotional and addictive behaviors. Neuroscience & Biobehavioral Reviews. August 2019;103:178-199. Available at https://www.sciencedirect.com/science/article/pii/S0149763418308613
Our research confirms an adverse effect of sugar intake from sweet food/beverage on long-term psychological health and suggests that lower intake of sugar may be associated with better psychological health. Knüppel A, Shipley MJ, Llewellyn CH, Brunner EJ. Sugar intake from sweet food and beverages, common mental disorder and depression: prospective findings from the Whitehall II study. Sci Rep. 2017;7(1):6287. Published 2017 Jul 27. doi:10.1038/s41598-017-05649-7. Available at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5532289/