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Health
Do extensively processed foods elevate the risk of Parkinson’s disease?

Alberto Ascherio, professor of epidemiology and nutrition at the Chan School of Public Health.
Stephanie Mitchell/Harvard Staff Photographer
New research indicates that individuals who consume larger portions are more likely to exhibit early indicators of the condition
Over half of the average American adult’s caloric intake derives from extensively processed foods, which provide minimal nutritional benefits and frequently include synthetic additives. An increasing amount of studies indicate that consuming significant quantities of these foods may heighten the risk of various chronic health issues. Recent findings associate high intake with a greater probability of displaying signs that precede Parkinson’s disease.
Investigators at Fudan University in Shanghai, China, in partnership with Alberto Ascherio from the Harvard T.H. Chan School of Public Health, utilized self-reported dietary information from over 40,000 health professionals, tracked since the mid-1980s. During the 2010s, participants also responded to queries regarding early non-motor signs associated with Parkinson’s.
By comparing these data points, the team discovered that individuals who ingested approximately 11 servings of extensively processed foods daily were 2.5 times more likely to exhibit early non-motor signs than those who consumed roughly two to three servings.
In this edited dialogue, Ascherio discusses the significance of this discovery and what remains unclear.
Before this study, what was the understanding of how nutrition may influence brain health, especially concerning neurodegenerative conditions like Parkinson’s?
It’s clear that nutrition holds importance. Indeed, there’s a general agreement that maintaining physical activity and a nutritious diet could delay the onset of several neurodegenerative ailments. However, much remains to be elucidated, particularly regarding Parkinson’s, which stands out among chronic diseases. For instance, cigarette smoking correlates with a diminished risk of Parkinson’s — it is one of the very few conditions where smoking does not elevate the disease’s risk. Ideally, the diet that aids in preventing cardiovascular diseases or cancer would also help in warding off Parkinson’s. Nonetheless, we do not have conclusive answers yet.
We have identified certain elements. Previous research has established that caffeine consumption is associated with a lower risk of Parkinson’s disease. Evidence suggests that the Mediterranean diet, known for lowering risks of various chronic diseases, might similarly benefit Parkinson’s, although the correlation isn’t as definitive as with heart conditions or diabetes. Additionally, the intake of flavonoids, a component found in fruits and vegetables, tends to show a moderate association with reduced risk of Parkinson’s. I believe we are still overlooking certain aspects. However, this examination of extensively processed food revealed significantly stronger associations than previously observed.
Why did you concentrate on early indications instead of those who developed Parkinson’s? And why focus on extensively processed foods?
The onset of Parkinson’s disease generally occurs at least 10 to 15 years prior to diagnosis. If one studies individuals with diagnosed Parkinson’s, they are essentially examining signs 15 years too late. Thus, we aimed to investigate which elements might affect the development of Parkinson’s disease. For this goal, we established this large cohort to evaluate the presence of what we refer to as prodromal features of Parkinson’s disease, which manifest many years prior to the typical indicators of the condition.
In regard to the dietary component, we’ve been analyzing nutrients and dietary patterns for many years, but more recently, the focus has shifted to assessing food based on the extent of processing and synthetic ingredients. Food processing has traditionally been essential for preservation and shelf life, but with extensively processed foods, we are addressing a different concern. This speaks more to an industrial approach aimed at enhancing food appeal rather than merely preserving it, linking it more to the marketing and commercial sides of the food sector.
Which prodromal features or early indications did you examine?
Given our substantial cohort, we chose from the clinical literature those common prodromal features that are relatively straightforward to evaluate with simple questions or cost-effective tests. One aspect was dream enactment, which we only inquired of participants with a sleep partner who could confirm it. Another was hyposmia, or a diminished sense of smell, which was assessed using a scratch-and-sniff test we mailed out. Additionally, we examined intestinal constipation, which is a non-specific feature but can become significant when noted alongside other signs.
When considering these features individually, they are quite prevalent, but the combination of three or more appears in only around 2 percent of older adults. Prior research has shown that individuals exhibiting all three of these signs are 23 times more likely to develop Parkinson’s disease.
“Will reducing the intake of these foods be adequate to prevent Parkinson’s? Almost certainly not, but it may be advantageous. To date, the most compelling evidence for lowering Parkinson’s risk pertains to physical activity.”
You established a correlation, but not necessarily a causation. How probable is it that extensively processed food is causing the emergence of the prodromal features?
This is quite complex. There’s always the possibility of reverse causality, where the prodromal features alter the diet instead of the other way around. For example, if someone experiences constipation, they may increase their fruit and vegetable intake to alleviate it. Nevertheless, we attempted to mitigate this by examining…
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diet quite early on. We commenced evaluating the prodromal characteristics in 2012, and we discovered that there’s already a connection between those characteristics in 2012 and the diet from 1986. In other terms, if you have a high intake of ultra-processed foods in 1986, you’re more prone to exhibit these prodromal traits in 2012. If it were reverse causation, one wouldn’t anticipate an association to exist that early.
The other limitation is what we refer to as confounding: Could the intake of ultra-processed foods serve as an indicator or correlate of something else? We attempt to adjust for various factors, but the adjustment is never flawless or exhaustive. We still do not know whether there’s something harmful in the ultra-processed foods, or perhaps, considering they contribute 50 percent or more of your caloric intake, you’re merely lacking other dietary components that offer protection.
If ultra-processed food is the trigger, what could the mechanism be?
We are not entirely sure. However, there is evidence that certain chemicals may induce Parkinson’s disease. The evidence is especially robust regarding pesticides and herbicides. It’s evident that they can heighten risk; we just don’t know which pesticides are responsible for that. This is due to our exposure to mixtures of pesticides and herbicides, rather than isolated substances.
Here, we find ourselves in a similar predicament. We can observe that ultra-processed food correlates with a higher prevalence of these prodromal features, but we genuinely do not know which component it is. And, as I mentioned earlier, it could even be a matter of nutrient displacement rather than a specific toxic influence.
What actions should individuals take with this knowledge?
Well, in light of the accumulated evidence concerning the risks of cardiovascular disease, diabetes, chronic decline, and dementia, it’s unquestionably clear that we should minimize the consumption of ultra-processed foods as much as feasible. Furthermore, it appears that Parkinson’s follows a similar trajectory. Will reducing these foods suffice to avert Parkinson’s? Almost certainly not, but it might be advantageous. Up until now, the most compelling evidence for decreasing Parkinson’s risk pertains to physical activity. I understand it’s somewhat disheartening not to have a definitive answer. It’s a very challenging question to tackle, but it’s one that we will keep investigating.
This research received partial funding from the NIH National Institute of Neurological Disorders and Stroke and the Department of Defense.