We’ve long known that some environmental exposures, notably pesticides, are associated with increased risk of Parkinson’s disease (PD). A new study is getting much media attention for sharing findings that link milk consumption to PD in a male Hawaiian population most likely through dairy contamination with pesticides.

The study population is from the Honolulu-Asia Aging Study, which followed men from midlife. Many chose to donate their brains after death. This study, published in Neurology, looked at data on milk intake collected from 1965 to 1968 and then examined the donated brain tissue.

Researchers found that loss of neurons in the substantia nigra (part of the brain associated with Parkinson’s) was highest in people who did not smoke and who consumed greater amounts of milk. They also correlated milk intake to brain levels of a pesticide called heptachlor epoxide, which was found in the milk supply in Hawaii in the early 1980s.

We spoke to Caroline Tanner, MD, PhD, director of the Parkinson's Disease Research Education and Clinical Center at the San Francisco Veteran's Affairs Medical Center; professor in residence at the University of California, San Francisco; member of the MJFF Scientific Advisory Board; and an author on the paper.

The Michael J. Fox Foundation: This is a very valuable study population. What more can you tell us about them?

Dr. Caroline Tanner: It’s one of the few human populations where we have information on diet and lifestyle and environmental exposures starting in midlife. We also examined them regularly to determine who has Parkinson’s, and many of them have agreed to donate their brains when they die. So we have been able to compare information about lifestyle and work and diet to their brains and their clinical characteristics, including parkinsonism and cognitive impairment. It’s a really valuable population because we almost never have the opportunity to look at all that together.

MJFF: What did you find in this study connecting dairy intake and Parkinson’s disease?

Dr. Tanner: We saw that certain pesticides that are lipid-soluble were more common in the brains of people who had Parkinson’s disease. And we also were able to look in the same population and see that people who had a higher intake of dairy products had a higher risk of Parkinson’s disease. So we put this all together, and we saw a relationship between milk intake and neuronal loss in the substantia nigra even in people who prior to death didn’t have a diagnosis of Parkinson’s.

It suggests that this population could have had an exposure to milk that could have been contaminated, but we can’t definitely make that conclusion because we don’t have samples of the milk these people drank. We do know that there was quite a concern in Hawaii when they realized that the food being given to the cows was derived from these pesticide-exposed end products and that was concentrating in milk.

MJFF: This data on milk consumption was gathered in the 1960s and regulations on heptachlor were set in the 1980s. What do these findings mean for today’s milk supply?

Dr. Tanner: As these things are recognized as harmful, there is more regulation. But some are persistent in the environment, so people can still be exposed to them. One would assume exposure would progressively diminish over time, but some chemicals may take a longer period of time. So where does that leave us? I think that probably people drinking milk in the United States today are not going to be exposed to a high dose of pesticides.

However, there still are a lot of chemicals in our environment that are unregulated and not very much work trying to investigate the relationship between diet, lifestyle, and environmental exposures and risk of parkinsonism. So to the individual: alarm is not indicated, and moderate intake, possibly using organic products that have more attention to what kinds of things animals are eating, would be a reasonable and prudent course.

From the scientific perspective, I think this study highlights the importance of having information on environmental factors that can be looked at in understanding disease risk. If we don’t have that information, we can’t recognize the association, and we can’t have the kind of regulatory reactions that we need to protect human health.

MJFF: Some of your previous work showed a relationship between genetic variants and increased risk from pesticide exposure. What do we know about the genetic role in converting from environmental exposure to Parkinson’s disease?

Dr. Tanner: Generally what we found is that variants in genes that in one way or another affect the way the body metabolizes or detoxifies pesticides can lead to higher risk of disease. This hasn’t yet been looked at in the Honolulu population that’s published here, but work in other populations suggests that it’s a combination of your genetic susceptibility and your environmental exposure that can influence your risk of Parkinson’s disease.

In the majority of cases of Parkinson’s there’s not a single gene cause and there’s not a single environment cause. It’s a combination of those things together that determine people’s risk of disease.

MJFF: Why is it that smokers were at a lower risk of Parkinson’s despite their milk intake?

Dr. Tanner: We’ve long known that nicotine exposure has an inverse relationship to disease risk. In fact there is a study testing the protective effect of nicotine in people recently diagnosed with Parkinson’s. An important note, though, is that no one should take up smoking to avoid PD. This same Honolulu population actually showed us a similar inverse relationship with high levels of uric acid, and there is also a trial testing an agent to raise levels in people with PD. And while standardized measures of physical activity weren’t collected in this study, we know that, too, protects from Parkinson’s disease.

So we know there are harmful things like pesticides and protective things like exercise and there is genetic predisposition. It is a complex picture, and we need more studies like this to identify those factors.

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