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A study links high ultraprocessed food consumption to increased risks of nonmotor Parkinson's disease symptoms, highlighting potential dietary impacts on neurodegeneration.
Xiang Gao, MD, PhD
A longitudinal study of more than 42,000 participants revealed that individuals who consume more ultraprocessed foods (UPFs) had higher odds of developing nonmotor prodromal Parkinson disease (PD) features, such as constipation, REM sleep behavior disorder (pRBD), and excessive daytime sleepiness (EDS), among others. Investigators concluded that more data is needed to see whether lowering UPF consumption may prevent the occurrence of nonmotor symptoms that often precede PD diagnosis.1
The analysis, comprising patients (n = 42,853) without a history of PD from the Nurses Health Study (NHIS) and Health Professionals Follow-Up Study (HPFS), collected data on UPF consumption from 1984-2006 through food frequency questionnaires. Led by Xiang Gao, MD, PhD, Distinguished Professor and Dean of Institute of Nutrition, Fudan University, data on pRBD and constipation was collected in 2012, while 5 additional nonmotor features were added and evaluated between 2014 and 2015 in a subset of patients. Published in Neurology, the primary outcome was the combination of all 7 prodromal features and further categorized as 0 (reference), 1, 2, and at least 3 features.
All in all, the results using multinominal logistic regression showed a trend with UPF consumption and the increasing number of PD prodromal features. When comparing extreme quintiles of cumulative average UPF consumption, the multivariable-adjusted OR for having at least 3 vs 0 prodromal PD features was 2.23 (95% CI, 1.61-3.20; P <.0001).
"To our knowledge, this study provides initial evidence that high UPF consumption may increase the risk of nonmotor features suggestive of prodromal PD," Gao et al wrote.1 "The biological mechanisms underlying UPF consumption and prodromal PD features are likely complex and multifactorial. UPFs tend to contain more added sugar, sodium, and saturated or trans-fat but less dietary fiber, protein, and micronutrients."
Additional data from the pooled multivariable-adjusted analysis revealed an OR of 1.58 (95% CI, 0.89-2.81; P heterogeneity = 0.02; P trend = 0.13) for having 2 vs 0 prodromal PD features and 1.57 (95% CI, 1.25-1.97; P heterogeneity = 0.30; P trend <.0001) for having 1 feature vs 0 prodromal PD features. Over the years, the odds for having at least 3 vs 0 prodromal features comparing extreme quintiles continued to climb, with ORs of 1.50 for UPF measured in 1986, 1.83 for UPF measured in 1990, 1.87 for UPF measured in 1994, 2.04 for UPF measured in 1998, 1.72 for UPF measured in 2002, and 2.54 for UPF measured in 2006.
In the study, investigators observed a notable finding, as higher intake of certain UPF groups like sauces, spreads, or condiments led to increased risk of prodromal PD features. In addition, other foods like packaged snacks or desserts; artificially or sugar-sweetened beverages; animal-based products; yogurt or dairy-based desserts; and packaged savory snacks, also had elevated risks.
Overall, the study continues to add to the growing body of evidence that supports the adverse effects of UPF consumption on neurodegenerative diseases. The study did have several limitations, including the fact that it focused on prodromal markers rather than clinical PD diagnoses, though these features are predictive of future PD.
Reverse causation was considered possible, as individuals with early PD symptoms may have altered their diets; however, lagged and baseline analyses suggested this did not fully account for the findings. Dietary data were self-reported via food frequency questionnaires, introducing measurement error, and categorization into Nova processing groups may be imprecise, the authors noted. Residual confounding was possible, and the homogenous study population (mostly White health professionals) limited the generalizability to more diverse groups.
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