Blood sugar levels after meals may matter for brain health later in life, according to a new study that examined genetic links between glucose regulation and Alzheimer’s disease risk.
Researchers from the University of Liverpool analyzed genetic and metabolic data from more than 350,000 adults enrolled in the UK Biobank. Their findings, published in Diabetes, Obesity and Metabolism, suggest that higher post-meal blood sugar levels are associated with a substantially increased risk of developing Alzheimer’s disease.
Previous research has consistently linked type 2 diabetes, insulin resistance and chronic high blood sugar to poorer cognitive outcomes. However, it has remained unclear which aspects of glucose metabolism may play the most direct role in dementia risk.
To explore this question, the researchers used a method called Mendelian randomisation, which leverages naturally occurring genetic differences to test whether certain biological traits are likely to have a causal relationship with disease. The team focused on genetic markers associated with fasting glucose, insulin levels and blood sugar measured two hours after eating.
The strongest association emerged for postprandial, or post-meal, blood sugar. Genetically predicted higher post-meal glucose levels were linked to a 69% higher risk of Alzheimer’s disease. The researchers did not find evidence that this association was driven by overall brain size or white-matter damage, suggesting that more subtle biological pathways may be involved.
“This finding could help shape future prevention strategies, highlighting the importance of managing blood sugar not just overall, but specifically after meals,” said Andrew Mason, lead author of the study.
Senior author Vicky Garfield emphasized the need for caution in interpreting the results.
“We first need to replicate these results in other populations and ancestries to confirm the link and better understand the underlying biology,” she said. “If validated, the study could pave the way for new approaches to reduce dementia risk in people with diabetes.”
The authors stress that the findings do not mean occasional blood sugar spikes cause Alzheimer’s disease. Instead, the study points to long-term patterns in how the body regulates glucose after eating as a potential contributor to dementia risk.
Because the analysis relied on genetic data rather than direct dietary measurements, the study does not identify specific foods or eating patterns responsible for higher post-meal glucose levels. Further research will be needed to determine how lifestyle, diet quality and medical management interact with post-meal blood sugar responses to influence brain health over time.
The study was supported by fellowships and public research funding focused on metabolic and population health, including a Professor David Matthews Non-Clinical Fellowship, a Wellcome Senior Research Fellowship and support from the UK National Institute for Health and Care Research.