Limited evidence suggests that MD adherence may be protective for Parkinson’s disease risk. Mechanistically, plant polyphenols may activate similar molecular pathways as caloric restriction diets, which helps explain the neuroprotective properties of the MD.
By Hannah Gardener and Michelle R. Caunca
Evidence for cognitive disorders is abundant, but there is a dearth of literature for other neurodegenerative disorders and for markers of neurodegeneration.
Further research is needed to elucidate the protective role of MD on neurodegeneration, the most salient components of the MD, and the most sensitive time periods over the lifecourse at which the MD may exert its effects.
Neurodegenerative diseases constitute a significant proportion of the neurological public health burden worldwide, with Alzheimer’s and Parkinson’s diseases predominantly affecting the aging population.
Alzheimer’s disease (AD) is the most common neurodegenerative disease and is expected to affect 13.8 million people by 2050, approximately a threefold increase from current-day prevalence estimates. Parkinson’s disease (PD) is the second most common neurodegenerative disorder and currently affects approximately 315 people per 100,000. With currently no curative therapies available for the treatment of neurodegenerative diseases, research efforts have shifted to identifying targets for prevention.
Modification of lifestyle and health behaviors, such as diet, are particularly effective public health targets for disease prevention. Given the association between cardiovascular and brain health, researchers posit that well-established cardioprotective dietary patterns, such as the Mediterranean-style diet (MD), may be protective for neurodegenerative diseases.
This review examines the most current literature on the association of the MD and neurodegeneration.
Conclusions
Although the past 5 years have yielded growing evidence in support of the MD in the prevention of cognitive impairment and dementia, the evidence remains inconclusive, with many questions left to be answered. Inconsistencies in the literature may be due to differences in the cognitive outcomes included (age-related cognitive decline, MCI, overall dementia, and AD).
Cognitive decline and dementia are etiologically heterogeneous outcomes, with vascular and non-vascular origins, which makes the identification of protective factors challenging. Also, adherence to the MD is typically a cohort-dependent variable, and a given individual may score high in one study population and low in another population where objective adherence to a MD is more prevalent. Differences in study populations by country of original, race/ethnicity, sex, and associated risk factors may also play a role, as there is limited information about effect modifiers for the relationship between MD and cognition.
Other factors that may account for inconsistencies across the literature include bias due to residual confounding by measured and unmeasured associated lifestyle factors (e.g., physical activity, sleep, social isolation, depression), differential and non-differential misclassification of diet based on self-report, and limited follow-up and small sample size resulting in insufficient statistical power.
Some studies on cognition are also lacking multiple neuropsychological assessments over time, needed to understand how diet can impact cognitive trajectories.
Evidence is mounting that the etiologically sensitive period for determining late-life cognitive health is mid-life, and perhaps even early-life. Dietary behavior in late-life, a few years before the age of diagnosis, may be too late to attenuate neurodegeneration.
Mid-life obesity, particularly, abdominal obesity, has been shown to be a well-established risk factor for dementia and cognitive decline, while the data for late-life obesity is inconsistent and inconclusive, underscoring the fact that mid-life may be the critical period during which diet may impact future neurodegeneration.
Late-life dietary habits may only be associated with cognitive outcomes to the extent that they are highly correlated with mid-life dietary habits. Ideally, future studies are needed that measure diet in mid-life (or even early-life), with repeated diet assessments over time, and follow participants for several decades until they reach the age when cognitive decline is measurable and dementia is diagnosed. In other words, long-term longitudinal follow-up studies are needed to help identify when during the lifecourse diet may have the greatest impact on late-life cognition and whether improvements in diet during mid-life or late-life have the potential to protect brain health and minimize neurodegeneration.
These are the crucial questions that need to be answered in future studies.
