Artificial sweeteners and risk of incident cardiovascular disease and mortality: evidence from UK Biobank
Authors' conclusion
Our findings suggest significant or marginally significant associations between artificial sweeteners and CVD and its subtypes (CAD, PAD, and HF). The associations are independent of genetic predisposition and are mediated primarily by T2DM. Therefore, the large-scale application of artificial sweeteners should be prudent, and the responses of individuals with different characteristics to artificial sweeteners should be better characterized to guide consumers' artificial sweeteners consumption behavior.
Study context
- Population
- UK Biobank participants free of cardiovascular disease (CVD) and diabetes at recruitment
- Participants
- 133,285 participants
- Exposure
- Artificial sweetener intake
- Outcome
- Incident CVD (overall and subtypes) and CVD mortality
Methodological detailsUK Biobank, repeated 24-hour diet recalls, Cox proportional hazard models, polygenic risk score, time-dependent mediation analysis
- UK Biobank
- Repeated 24-hour diet recalls
- Cox proportional hazard models
- Polygenic risk score
- Time-dependent mediation analysis
Main finding
As reported in the abstract
Each teaspoon increase, as printed
Observational data: associations, not effects.
Further findings
Stratified analyses
- Non-whites were at greater risk of incident overall CVD from artificial sweetener
- People with no obesity (BMI < 30 kg/m²) tended to be at greater risk; obesity interaction not significant
Genetic susceptibility (polygenic risk score (PRS))
- CVD risk independent of genetic susceptibility; no significant additive or multiplicative interaction
Mediation by prior T2D
- Proportion of indirect effect, overall CVD
- 70.0%
- Proportion of indirect effects, coronary artery disease (CAD), peripheral arterial disease (PAD) and heart failure (HF)
- 68.2 to 79.9%
Original publication
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