Disentangling the relationship between glucose, insulin and brain health: A UK Biobank study
Authors' conclusion
The association between elevated 2-h post-load glucose and increased Alzheimer's risk supports a potential role for postprandial hyperglycaemia in dementia. The lack of associations between fasting or postprandial glucose and hippocampal, total-brain or white matter hyperintensity volumes suggests this risk may operate independently of gross structural atrophy.
Study context
- Population
- UK Biobank, White British, mean age 56.9 years, 54% femalemaximum N
- Participants
- 357,883 participants
- Comparison
- Genetically proxied glycaemic traits and brain health
- Outcome
- Alzheimer's dementia risk per higher 2-h post-load glucose
Methodological detailsinverse-variance weighted Mendelian randomisation (MR) as main estimator, MR-Egger, weighted median estimator and Mendelian Randomization Pleiotropy RESidual Sum and Outlier (MR-PRESSO) sensitivity tests, replication in an independent Alzheimer's dementia genome-wide association study (GWAS)
- Inverse-variance weighted MR as main estimator
- MR-Egger, weighted median estimator and MR-PRESSO sensitivity tests
- Replication in an independent Alzheimer's dementia GWAS
Main finding
As reported in the abstract
Higher 2-h post-load glucose and Alzheimer's dementia risk, OR
1.69 (1.38-2.07) (95% CI)
Increased Alzheimer's dementia risk
69%
Further findings
- Fasting insulin, fasting glucose and postprandial glucose did not influence total brain, hippocampal or white-matter hyperintensity volumes
Original publication
Disentangling the relationship between glucose, insulin and brain health: A UK Biobank study. Diabetes Obes Metab. Published 12 December 2025. doi:10.
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