ArticlePloS one2024
Associations between artificial sweetener intake from cereals, coffee, and tea and the risk of type 2 diabetes mellitus: A genetic correlation, mediation, and mendelian randomization analysis.
Article in PloS one, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 13 citations in OpenAlex.
- Association of sugar-sweetened, artificially sweetened, and unsweetened tea with all-cause and cause-specific mortality: a prospective cohort study in UK biobank.BMC public health · 2025Article
- Associations of breakfast cereal consumption with all-cause and cause-specific mortality: a large-scale prospective analysis.Nutrition journal · 2025Article
- An integrative analysis reveals cancer risk associated with artificial sweeteners.Journal of translational medicine · 2025Article
- Synthetic vs. non-synthetic sweeteners: their differential effects on gut microbiome diversity and function.Frontiers in microbiology · 2025Article
- Artificial Sweetener and the Risk of Adverse Pregnancy Outcomes: A Mendelian Randomization Study.Nutrients · 2024Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPrevious studies have emphasized the association between the intake of artificial sweeteners (AS) and type 2 diabetes mellitus (T2DM), but the causative relationship remains ambiguous.
methodsThis study employed univariate Mendelian randomization (MR) analysis to assess the causal link between AS intake from various sources and T2DM. Linkage disequilibrium score (LDSC) regression was used to evaluate the correlation between phenotypes. Multivariate and mediation MR were applied to investigate confounding factors and mediating effects. Data on AS intake from different sources (N = 64,949) were sourced from the UK Biobank, while T2DM data were derived from the DIAbetes Genetics Replication And Meta-analysis.The primary method adopted was inverse variance weighted (IVW), complemented by three validation techniques. Additionally, a series of sensitivity analyses were performed to evaluate pleiotropy and heterogeneity.
resultsLDSC analysis unveiled a significant genetic correlation between AS intake from different sources and T2DM (rg range: -0.006 to 0.15, all P < 0.05). After correction by the false discovery rate (FDR), the primary IVW method indicated that AS intake in coffee was a risk factor for T2DM (OR = 1.265, 95% CI: 1.035-1.545, P = 0.021, PFDR = 0.042). Further multivariable and mediation MR analyses pinpointed high density lipoprotein-cholesterol (HDL-C) as mediating a portion of this causal relationship. In reverse MR analysis, significant evidence suggested a positive correlation between T2DM and AS intake in coffee (β = 0.013, 95% CI: 0.004-0.022, P = 0.004, PFDR = 0.012), cereal (β = 0.007, 95% CI: 0.002-0.012, P = 0.004, PFDR = 0.012), and tea (β = 0.009, 95% CI: 0.001-0.017, P = 0.036, PFDR = 0.049). No other causal associations were identified (P > 0.05, PFDR > 0.05).
conclusionThe MR analysis has established a causal relationship between AS intake in coffee and T2DM. The mediation by HDL-C emphasizes potential metabolic pathways underpinning these relationships.
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