Sweet Tooth, Faster Aging: Dietary Preferences Linked to Dementia Risk

A sweeping analysis of data from the UK Biobank has revealed a striking pattern: people whose food preferences cluster around sweets and sugary items appear to face a dramatically elevated risk of developing dementia, and the connection seems to run through the very machinery of biological aging. The study, published in the journal GeroScience, tracked participants over years of follow-up and found that those with a so-called sweet-tooth dietary preference profile had a 79 percent higher risk of all-cause dementia compared with people whose preferences aligned with healthier eating patterns. The elevated risk extended to specific forms of the disease as well, with a 62 percent higher risk of Alzheimer’s disease and an even more pronounced 202 percent higher risk of vascular dementia among the sweet-tooth group. These figures, derived from prospective cohort analysis rather than retrospective recall, add considerable weight to a growing body of evidence linking dietary habits to long-term brain health.

The research team, led by Mengtong Sun and Qida He of City University of Hong Kong along with colleagues at institutions in China and the United States, took an approach that differs from most nutritional epidemiology. Rather than asking participants to estimate how much of each food they ate, the investigators analyzed food preference questionnaire data, capturing what people actually like to eat. Using a statistical technique known as latent profile analysis, they sorted participants into distinct dietary preference profiles based on the overall pattern of their food likes and dislikes. This method identified three coherent groups: a health-aligned profile, a broad-preference profile in which participants reported liking most foods across the spectrum, and a sweet-tooth profile characterized by strong preferences for sugary items.

Latent profile analysis is a person-centered modeling approach that treats the population as a mixture of unobserved subgroups, each with its own characteristic response pattern. Instead of reducing diet to a single score, the method allows researchers to discover natural clusters of preference that may correspond to real-world eating styles. This is a meaningful departure from the food frequency questionnaires that have long dominated dietary research and that have drawn criticism for their reliance on memory and their limited ability to capture the complexity of habitual intake. Preference data, while not a direct measure of consumption, offers a stable and psychologically grounded window into dietary behavior, and previous work in twin cohorts has shown that food preference patterns are partly heritable and reasonably reproducible over time.

To connect dietary preference with dementia, the team employed Cox proportional hazards models, the standard tool for analyzing time-to-event data in cohort studies. These models estimated the association between each dietary preference profile and the risk of incident dementia while accounting for the interaction between diet and genetic susceptibility. Genetic risk was characterized using polygenic risk scores, which aggregate the effects of thousands of genetic variants into a single measure of inherited predisposition. The results showed not merely an independent effect of the sweet-tooth profile but a significant additive interaction: among individuals with high genetic susceptibility to dementia, the sweet-tooth preference amplified risk beyond what would be expected from either factor alone. In other words, the people least equipped biologically to tolerate a sugar-heavy dietary pattern were the ones most harmed by it.

Perhaps the most technically ambitious component of the study was its effort to quantify biological aging. The researchers computed two distinct measures of biological age from blood chemistry and organ function markers. The first, the Klemera-Doubal method biological age, or KDM-BA, is an algorithm that combines multiple biomarkers into an estimate of physiological age, allowing researchers to calculate how much faster or slower an individual is aging relative to their chronological peers. The second, phenotypic age or PhenoAge, was developed using data from the NHANES survey and has been validated as a predictor of morbidity and mortality across diverse populations. As a third marker, the team measured leukocyte telomere length, the length of protective DNA-protein structures at the ends of chromosomes in white blood cells, which typically shortens with cell division and chronic biological stress. Telomere length was available for hundreds of thousands of UK Biobank participants through high-throughput measurement.

The sweet-tooth profile was associated with acceleration on all three markers: faster KDM-BA, faster PhenoAge, and shorter leukocyte telomeres. This convergence across independent measures of aging is notable because each captures a different facet of the aging process. KDM-BA and PhenoAge reflect systemic physiological decline as expressed in blood-based biomarkers, while telomere length reflects cellular replicative history and cumulative inflammatory and oxidative stress. That a single dietary preference pattern correlates with all three suggests that the sweet-tooth profile is not merely a marker of some isolated metabolic quirk but is entangled with the broader biology of aging itself. Prior research has already linked accelerated biological aging, measured with these same tools, to increased dementia incidence in the UK Biobank, providing a plausible mechanistic bridge between diet and disease.

To test that bridge formally, the investigators conducted mediation analysis, a statistical framework for estimating how much of the association between an exposure and an outcome flows through an intermediate variable. The exploratory results indicated that the biological aging markers statistically accounted for between 2.28 and 4.82 percent of the observed association between sweet-tooth preference and dementia risk. The authors are careful about the interpretation here, and appropriately so. The mediation proportion is modest, which means that accelerated biological aging explains only a small fraction of the diet-dementia link, leaving the majority of the association to be explained by other pathways. Candidate mechanisms discussed in the broader literature include chronic neuroinflammation, disturbances of the brain-gut-microbiome axis, glucoregulatory stress, and vascular injury, each of which has been implicated in both high-sugar dietary patterns and neurodegeneration. The researchers also note that mediation analysis in observational data is inherently exploratory and cannot establish causal chains with certainty.

The study’s scale and design lend it credibility. It was conducted within the UK Biobank, a resource of roughly half a million middle-aged and older adults in the United Kingdom who have undergone extensive baseline assessment, including dietary questionnaires, physical measurements, blood sampling, and whole-genome genotyping. The cohort design followed participants forward in time, which reduces but does not eliminate the risk of reverse causation, the possibility that preclinical disease influences dietary preference rather than the other way around. The investigators followed reporting guidelines for observational epidemiology, applied competing-risk methods where appropriate, and adjusted for a range of confounders. Still, as with any observational study, unmeasured confounding remains possible, and food preference data capture liking rather than measured intake, so some uncertainty about the exact dietary behaviors driving the association is unavoidable.

What makes the findings compelling is their consistency with an expanding literature on diet and brain health. Mediterranean, DASH, and MIND dietary patterns have each been associated with lower dementia risk and favorable brain structural markers in prior cohort studies, and adherence to the EAT-Lancet planetary health diet has been linked to slower biological aging and longer life expectancy in UK Biobank analyses. Conversely, high consumption of ultra-processed foods and sugary beverages has been tied to adverse brain outcomes and accelerated aging, with some evidence that genetic risk modifies these relationships. The new study extends this work by shifting the analytical lens from nutrient and food-group intake to the underlying architecture of food preference, and by explicitly modeling the interplay between diet, genetic susceptibility, and biological aging within a single framework.

The practical implications are targeted rather than universal. Because the additive interaction showed that the sweet-tooth profile was most dangerous among genetically susceptible individuals, the authors argue for dietary interventions aimed specifically at people at elevated inherited risk of dementia. For that population, curbing sugar-centric preferences and shifting toward health-aligned eating could represent a modifiable lever at a stage of life when prevention is still possible. The researchers stop short of claiming that changing preferences alone would eliminate risk, and the modest mediation share cautions against viewing biological aging as the sole pathway. But the study adds a vivid and quantifiable dimension to an old piece of advice: what you like to eat may shape not just your waistline but the pace at which your body and brain grow old, and for those carrying genetic risk, a sweet tooth may be a warning worth heeding.

Subject of Research: Association between dietary preference profiles, biological aging markers, and incident dementia risk in a prospective UK Biobank cohort

Article Title: Dietary preference, biological aging, and incident dementia: a prospective cohort study

Article References: Sun, M., Huang, F., Sun, N., Ding, H., Shi, F., Wang, S., Yao, J., & He, Q. (2026). Dietary preference, biological aging, and incident dementia: a prospective cohort study. GeroScience. https://doi.org/10.1007/s11357-026-02567-3

Image Credits: AI Generated

DOI: 10.1007/s11357-026-02567-3

Keywords: dementia, dietary preference, biological aging, UK Biobank, sweet tooth, Alzheimer's disease, vascular dementia, telomere length, PhenoAge, polygenic risk score, cohort study, nutrition