Диета, богатая флавоноидами, снижает риск болезни Паркинсона: исследование

From tea and berries to dark chocolate, researchers tracked how a flavonoid-rich dietary pattern relates to Parkinson’s disease risk and explored the biological signals that might help explain the connection. Flavonoid-rich dietary patterns and incident hospital-recorded Parkinson's disease: a prospective UK Biobank study. Image Credit: DIVA.photo / Shutterstock A dietary pattern higher in flavonoid-rich foods is associated with a modestly lower risk of incident hospital-recorded Parkinson’s disease, according to a new study published in the journal Frontiers in Nutrition. Background Parkinson’s disease (PD) is a progressive neurodegenerative disorder associated with physical disability, poor quality of life, and mortality. Despite the increasing global prevalence, effective disease-modifying therapies remain lacking. Among modifiable lifestyle factors, diet has gained significant attention in PD prevention research. Several healthy dietary patterns, including the Mediterranean diet and the Mediterranean-DASH Intervention for Neurodegenerative Delay (MIND), have been linked to a lower risk of PD. Flavonoids are a major subclass of dietary polyphenols, which are bioactive compounds widely found in plant-based foods, such as berries, citrus fruits, and tea. Studies investigating the health benefits of flavonoids have highlighted antioxidant, anti-inflammatory, and neuroprotective effects. Studies linking flavonoid intake to PD risk have produced inconsistent results. While some studies have indicated that higher anthocyanin intake is associated with lower PD risk, long-term follow-up studies have not found a clear inverse association between total flavonoid intake or individual flavonoid subclasses and PD risk. Given such discrepancies in findings, a team of researchers from China analyzed data from 123,655 UK Biobank participants to examine the association between intake of different types of flavonoid-rich foods and incident hospital-recorded PD. Furthermore, they linked UK Biobank plasma proteomic data to publicly available transcriptomic datasets to identify preliminary molecular and cellular context for this association. Key findings The researchers analyzed participant-reported data on habitual intake of 11 flavonoid-rich foods, including black tea, green tea, red wine, apples, berries, grapes, oranges, grapefruit, sweet peppers, onions, and dark chocolate. They identified a total of 796 incident hospital-recorded PD cases using UK Biobank-linked hospital inpatient and death registry data. The multivariable Cox proportional hazards analysis indicated that individuals with the highest flavonoid diet scores had a lower incidence of hospital-recorded PD compared to those with the lowest scores. However, no individual food source or flavonoid subclass remained significantly associated with incident PD after multiple-testing correction. The observed inverse association remained directionally similar after excluding incident PD cases occurring within the first 1–5 years of follow-up. However, the association was attenuated after excluding incident PD cases occurring within the first 6–10 years after baseline or after adjusting for coffee intake. To explore a possible biological context for this epidemiological association, the analysis of plasma proteomic data prioritized a signature comprising 20 protective-aligned proteins and 4 risk-aligned proteins that aligned with the observed inverse association. No individual protein remained significant after false discovery rate correction in either screening step, and functional enrichment was weak, although the nominally enriched terms were related to cell adhesion, transport, and immune processes. The mapping of these protein signatures in peripheral immune cells revealed that representative protective-aligned genes, including ITGAM and LGALS3, were expressed predominantly in monocytes and dendritic cells, whereas risk-aligned genes, including B2M and GZMB, were expressed at higher levels in NK/T-cell populations. The exploratory CellPhoneDB analysis suggested expression-inferred, predominantly protective-aligned, integrin-related interaction patterns involving ITGAM and ITGB2. In the external substantia nigra dataset, protective-aligned signature activity was relatively higher in astrocytes, with additional representation in endothelial cells and microglia, whereas risk-aligned signature activity was highest in T/NK cells. Furthermore, representative protective-aligned genes showed immune- and microglia-associated expression, whereas risk-aligned genes showed immune-associated expression. Study significance The study found that higher intake of flavonoid-rich foods is modestly associated with a lower risk of incident hospital-recorded PD. This inverse association was mainly observed among individuals with the highest flavonoid diet scores. In contrast to previous studies that investigated the effects of single nutrients or total flavonoid intake on PD risk, the current study emphasized the combined intake of flavonoid-rich foods. Previous studies using the same UK Biobank population have reported that greater diversity of flavonoid intake, independent of total quantity, is associated with lower risks of chronic and neurodegenerative diseases. The study found that the association persisted after adjustment for socioeconomic status, lifestyle, energy intake, PD-related genetic risk factors, and self-rated health. However, the association was no longer statistically significant after adjusting for coffee intake. Coffee consumption is itself associated with lower PD risk, while tea contributes to the FDS and overlaps with broader beverage patterns. The observed attenuation after coffee adjustment may therefore reflect residual confounding, exposure overlap, or overadjustment. PD is associated with a long prodromal phase, meaning that prodromal symptoms may appear years before diagnosis. These symptoms may alter dietary habits, highlighting the possibility of reverse causation. To reduce the risk of reverse causation, the study used progressively longer lag analyses, excluding PD cases occurring within the first 10 years of follow-up. Estimates were attenuated within the 6–10-year exclusion windows. Although this adjustment reduced the possibility of reverse causation, the influence of preclinical symptoms on diet cannot be entirely ruled out given the long prodromal phase. The study also relied on self-reported dietary data, while hospital and death-registry diagnoses may under-ascertain milder or outpatient-managed PD cases. The study participants were predominantly of European ancestry and healthier than the general population, raising the possibility of healthy-volunteer selection bias and potentially limiting the generalizability of the findings to other populations. The study's analysis of proteomic and transcriptomic data provides a biological context centered on neuroimmune and adhesion-related interfaces rather than evidence for a specific mechanism. Future studies should include demographically diverse populations, external validation, longitudinal dietary and proteomic measurements, brain-relevant multi-omics data, and functional experiments to understand the causal direction and biological basis of the association between flavonoid-rich dietary intake and PD risk.