Adherence to the MIND diet and longitudinal brain structural changes over a decade: evidence from the Framingham heart study offspring cohort

Background: The MIND diet was favourably linked to lower risk of neurodegenerative diseases. While previous cross-sectional studies implied its beneficial associations with brain imaging markers, its associations with long-term brain structural changes remained unclear. Methods: We included 1647 middle-aged and older individuals from the Framingham Heart Study Offspring cohort (FOS). MIND diet score was calculated from a validated FFQ, repeatedly administered at Exams 5, 6, and 7. Brain imaging markers were acquired between 1999 and 2019, with a median repetition (interquartile range, IQR) of 3 (2-3) times. We used linear mixed models to assess the associations of the MIND diet score and its components with longitudinal brain structural changes. Results: Over a median follow-up of 12.3 years (IQR 6.8–13.8 years), greater adherence to the MIND diet was associated with slower decline in total grey matter volume. Specifically, each three-unit increase in the MIND diet score was linked to a 0.279 cm³/year (95% CI 0.089 to 0.469) slower decline in total grey matter volume, corresponding to a 20.1% attenuation in age-related change that was equivalent to 2.5 years of reduced brain ageing during the 12.3-year follow-up. Additionally, higher MIND diet score was associated with slower increases in lateral ventricular volume (−0.071 cm³/year, 95% CI −0.125 to −0.017), notably in the left lateral ventricle (−0.041 cm³/year, 95% CI −0.070 to −0.013), reflecting approximately 8.0% and 8.8% attenuation of age-related changes, equivalent to roughly 1.0 year of delayed brain ageing during follow-up. Conclusions: In this prospective cohort study, greater adherence to the MIND diet was associated with slower brain structural atrophy, particularly regarding grey matter loss and ventricular enlargement. These findings support the potential of the MIND diet as a strategy to support brain health and delay structural brain ageing.