From practiceupdate.com.
Here is a link to the paper.
Here are some excerpts.
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OBJECTIVETo study the relationships between artificial sweeteners, accounting for all dietary sources(total and by type of artificial sweetener) and risk of type 2 diabetes (T2D), in a large-scale prospective cohort.
RESEARCH DESIGN AND METHODS
The analyses included 105,588 participants from the web-based NutriNet-Santé study (France, 2009-2022; mean age 42.5 ± 14.6 years, 79.2% women). Repeated 24-h dietary records, including brands and commercial names of industrial products, merged with qualitative and quantitative food additive composition data, enabled artificial sweetener intakes to be accurately assessed from all dietary sources. Associations between artificial sweeteners (total, aspartame, acesulfame potassium [K], and sucralose) and T2D were investigated using Cox proportional hazard models adjusted for potential confounders, including weight variation during follow-up.
RESULTS
During a median follow-up of 9.1 years (946,650 person-years, 972 incident T2D), compared with nonconsumers, higher consumers of artificial sweeteners (i.e., above the sex-specific medians of 16.4 mg/day in men and 18.5 mg/day in women) had higher risks of developing T2D (hazard ratio [HR] 1.69; 95% CI 1.45-1.97; P-trend <0.001). Positive associations were also observed for individual artificial sweeteners: aspartame (HR 1.63 [95% CI 1.38-1.93], P-trend <0.001), acesulfame-K (HR 1.70 [1.42-2.04], P-trend <0.001), and sucralose (HR 1.34 [1.07-1.69], P-trend = 0.013).
During a median follow-up of 9.1 years (946,650 person-years, 972 incident T2D), compared with nonconsumers, higher consumers of artificial sweeteners (i.e., above the sex-specific medians of 16.4 mg/day in men and 18.5 mg/day in women) had higher risks of developing T2D (hazard ratio [HR] 1.69; 95% CI 1.45-1.97; P-trend <0.001). Positive associations were also observed for individual artificial sweeteners: aspartame (HR 1.63 [95% CI 1.38-1.93], P-trend <0.001), acesulfame-K (HR 1.70 [1.42-2.04], P-trend <0.001), and sucralose (HR 1.34 [1.07-1.69], P-trend = 0.013).
CONCLUSIONS
Potential for reverse causality cannot be eliminated; however, many sensitivity analyses were computed to limit this and other potential biases. These findings of positive associations between artificial sweetener intakes and increased T2D risk strengthen the evidence that these additives may not be safe sugar alternatives. This study provides important insights in the context of on-going reevaluation of artificial sweeteners by health authorities worldwide.
The main model was adjusted for variables suspected or known to be associated with diet and with T2D. These variables pertained to the following domains: socio demographic (age, sex, and education), lifestyle (baseline physical activity, smoking status, and number of smoked cigarettes), health (family history of diabetes in first-degree relatives and prevalence of CVD, hypertension, or dyslipidemia), number of 24-h dietary records, and weight status (baseline BMI and mean percent age of weight change per year of follow up [calculated as the difference between end of follow-up weight and baseline weight divided by baseline-weight, multi plied by 100 and divided by follow-up time]).This variable was chosen for adjustment in the main models since it provided an overview of the weight trajectory across follow-up, to limit potential confounding or reverse causality associated with this key factor. The main model was also adjusted for food groups and nutrients for which a role in T2D etiology has been strongly suggested (27): energy intake without alcohol and daily intakes of alcohol, sugar, sodium, saturated fatty acids, fiber, fruit, vegetables, red/processed meat, and dairy products. Analyses by specific artificial sweeteners (i.e., aspartame, acesulfame-K, and sucralose) were additionally adjusted for other artificial sweetener intakes. Unless stated otherwise, covariables were measured at baseline.
Potential for reverse causality cannot be eliminated; however, many sensitivity analyses were computed to limit this and other potential biases. These findings of positive associations between artificial sweetener intakes and increased T2D risk strengthen the evidence that these additives may not be safe sugar alternatives. This study provides important insights in the context of on-going reevaluation of artificial sweeteners by health authorities worldwide.
The main model was adjusted for variables suspected or known to be associated with diet and with T2D. These variables pertained to the following domains: socio demographic (age, sex, and education), lifestyle (baseline physical activity, smoking status, and number of smoked cigarettes), health (family history of diabetes in first-degree relatives and prevalence of CVD, hypertension, or dyslipidemia), number of 24-h dietary records, and weight status (baseline BMI and mean percent age of weight change per year of follow up [calculated as the difference between end of follow-up weight and baseline weight divided by baseline-weight, multi plied by 100 and divided by follow-up time]).This variable was chosen for adjustment in the main models since it provided an overview of the weight trajectory across follow-up, to limit potential confounding or reverse causality associated with this key factor. The main model was also adjusted for food groups and nutrients for which a role in T2D etiology has been strongly suggested (27): energy intake without alcohol and daily intakes of alcohol, sugar, sodium, saturated fatty acids, fiber, fruit, vegetables, red/processed meat, and dairy products. Analyses by specific artificial sweeteners (i.e., aspartame, acesulfame-K, and sucralose) were additionally adjusted for other artificial sweetener intakes. Unless stated otherwise, covariables were measured at baseline.
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