Artificially Sweetened Beverages Beyond the Metabolic Risks: A Systematic Review of the Literature

We carried out a review of the available literature on the effects that artificially sweetened beverages (ASBs) such as diet soda (DS) have on health, particularly those not related to incident diabetes mellitus, obesity, and metabolic syndrome. A search of scientific articles was carried out using 11 different databases: PubMed, Cochrane, LILACS, MEDLINE Ovid, JAMA Network, IBECS, Cumed, Scopus, SciELO, MEDLINE-EBSCO, and Taylor & Francis Online. Articles published in the last 10 years were considered, considering cross-sectional studies, retrospective or prospective cohort studies, case-control studies, and randomized controlled clinical trials. Only articles in Spanish or English were considered using the MeSH (Medical Subject Heading) and DeCS (Descriptores en Ciencias de la Salud) terms, including “Diet soda,” “Health,” “Artificial sweetener,” “Gaseosa sin azúcar,” “Refresco sin azúcar,” and “Salud.” Additionally, Boolean operators “AND” and “Y” were used. A total of 1,323 articles were obtained in the initial search, of which 21 main ones were selected for review, which included the topic of DS consumption and explored the health consequences that it poses on different organs. The question of whether ASBs such as DS are a preferred substitute is becoming more and more important in terms of public policy due to mounting evidence of the potential negative health effects of their excessive consumption. This systematic review, the first of its kind to our knowledge, sheds light on how excessive DS consumption can affect multiple organ systems, and associations have been made to mental health burden, delays in child neurodevelopment, cardiac remodeling, worsening retinopathy in diabetics, incidental end-stage renal disease, non-Hodgkin's lymphoma and multiple myeloma in men, rheumatoid arthritis in women, hip fractures, dental erosion, increases in breath alcohol concentration when used in alcoholic beverages, and accelerated cell aging. Further studies should delve further to understand the pathophysiologic mechanisms of these associations.