Ask an Expert: Genetics, Environment, and Parkinson’s Disease

Dr. Beate Ritz received her MD and a PhD in Medical Sociology from the University of Hamburg Germany in 1983 and 1987; she was a research fellow and resident at the Psychiatric University-Hospital in Hamburg from 1987-1989, and received doctoral training and a PhD degree in Epidemiology in 1995 from the University of California at Los Angeles (UCLA). Upon graduation, she joined the faculty of the School of Public Health at UCLA and is currently Professor and Vice-Chair of the Epidemiology Department.

Dr. Ritz is also a member of the Center for Occupational and Environmental Health (COEH), the Southern California Environmental Health Science Center (SCEHSC) and co-directs the National Institute of Environmental Health Sciencesfunded UCLA Center for Gene-Environment Studies of Parkinson’s disease. She was one of the plenary speakers at Parkinson Society British Columbia’s most recent provincial conference, Moving Forward, Together, on June 3, 2017.


What are gene-environment interactions, and how have they been underexplored in Parkinson’s disease (PD) related research so far?

Gene-environment interactions (GxE) are the processes by which an individual person’s genetic make-up interacts with agents in the environment. These agents can include food and medications, mould, pesticides and air pollution, just to name a few. Even the smallest differences in genetic factors can change how an individual reacts to the environment around them. Almost all diseases are the result of GxE interactions.

Gene-environment interactions can be challenging to study since researchers need to both measure environment exposures reliably as well as determine the appropriate genes to examine. For example, one of the studies I was involved with determined that an increase in PD risk is associated with variations in the paraoxonase 1 – an enzyme also known as PON1 that breaks down pesticides that enter the human body – and dopamine transporter genes.

 

Can you tell us a bit about your research interests and how they pertain to PD?

My research focuses on the effects of both occupational and environmental toxins. Toxins such as pesticides and air pollution can impact neurodegenerative diseases and cancers. One of our major studies that garnered interest in Canada and the United States was a large-scale project in rural areas of Southern California. We used detailed information collected by a large group of patients with Parkinson’s in California’s Central Valley. I worked with a team of researchers to evaluate both genetic and environmental risk factors and how they interact in PD. This study established that the combination of the fungicide maneb and the herbicide paraquat can increase the risk of developing Parkinson’s disease by 75%. The earlier the exposure, the greater the risk of developing the disease. Furthermore, people who were exposed to paraquat, maneb and ziram (a fungicide) at work were three times as likely to develop Parkinson’s than those who were not exposed to these chemicals at all. I believe that it is very likely these pesticides work to lower peoples’ natural defenses to disease. The results of these investigations have provided a foundation for a number of other projects that evaluate pesticide exposure and genetic vulnerability.

 

Are all pesticides neurotoxic?

The short answer is some, but not all. Different pesticides may work in combination with each other. Insecticides are specifically designed to kill insects by targeting their nervous system. However, insecticides don’t distinguish between insects, people and animals, therefore insecticides, as well as some herbicides and fungicides, have been proven to have neurotoxic effects.

 

Can you briefly explain some of your research that focuses on occupations and lifestyle in Parkinson’s?

In 2016, I co-authored a study that concluded that individuals who engage in moderate to vigorous physical activity in youth are at the lowest risk of developing Parkinson’s disease. Particularly interesting was the finding that participation in competitive sports in youth seems to lower the risk of developing PD more than life-long physical activity. That being said, it could be possible that participating in sports and physical activity could be markers for pre-existing factors that lower risk already. It becomes a question of nature versus nurture. Right now, evidence is inconclusive whether exercise or genetics is a stronger protective factor.

 

What else would you like our readers to know about the direction of your work?

Parkinson’s disease is incredibly complex. I’m a strong believer that approaching its study from a cross-disciplinary approach is the most appropriate way to better understand the condition to improve treatment and potentially find a cure. However, community studies that focus on PD patients need to be an integral part of such research efforts. Currently, there are too few of them.

Only long-term studies of humans with PD can improve our understanding of how the disease progresses. By analyzing clinical symptoms of Parkinson’s, my team has concluded that our current method of classifying the symptoms of Parkinson’s disease – both motor and nonmotor – are grossly inadequate and do not provide sufficient reflections of health-related quality of life. Now, we are continuing to follow a large group of community-based patients to document different aspects of PD. This will provide a better understanding of the disease and eventually identify factors that affect its progression.

 

What drew you to study the health effects of occupational and environmental toxins on chronic diseases?

The ubiquitous exposure to neurotoxins delivered via a variety of means, such as air, soil, water contamination as well as pesticides, is unprecedented in human history. Similarly, the large aging population is much more vulnerable to these toxicants and will likely have to live with a diminished quality of life for many years. This is a looming public health crisis we need to address, now.

 

As a researcher who has worked with subjects who have been exposed to environmental risks, are you optimistic about policy changes that may protect communities from environmental toxins, or are current policies still worrisome for you?

I wish I could be more optimistic, but agricultural and chemical industries are very resistant to making changes. The current political climate in the US is certainly not in favour of expanding Environmental Protection Agency type regulatory efforts to reduce human pesticide exposures. I hope this trend will change as more scientific evidence of the harm done to human life accumulates.

 

Is there anything you would like to add about genetics, environment and Parkinson’s?

One myth that we should debunk is that ‘natural’ means harmless or non-toxic. The natural pesticide called rotenone – derived from an African tree root – has been used in organic farming because it is considered natural. It is, however, a strong toxicant that causes PD like symptoms in animals and has been shown to also be involved in the development of Parkinson’s in humans.

 


This content was published in the Summer 2017 edition of our quarterly magazine, Viewpoints. The content was accurate as of this publication date.


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