Here’s a study clearly demonstrating a positive relationship between insecticides and herbicides, but also commonly used solvent chemicals and the development of Parkinson’s syndrome.
Most people are exposed to herbicides and pesticides, not only farmers. Think of your home, school and park lawns, golf courses, driving past garden services at work in the streets and neighborhoods……….. Exposure to these chemicals increases your risk for developing Parkinsons Disease by 33% to 80%.
Testing for chemicals: In practice, it is not currently possible to assess how much chemicals you have in your body other than an exposure history. We do not have tests outside of the research setting. We can however use Autonomic Response Testing to determine which types of chemicals act as stressors on your system. Mercury and other toxic metals are also linked to PD, which can be very easily assessed and safely treated.
Treatment: Depending on the situation and combination of factors involved, there are safe, effective and economical means to decrease the effect of solvents, pesticides and herbicides on the body and to gradually support biochemical pathways that are responsible to clear these chemicals from the body. Tissue repair, cell membrane and dopamine support are also two other components considered.
Currently we do not have studies to guide us on expectations regarding improvement in PD when addressing these individual components, and eagerly await more scientific investigations. W.Vosloo ND MHom
Pesticide Exposure Tied to PD Risk
Exposure to pesticides and solvents appears to be a risk factor for Parkinson’s disease, a meta-analysis found.
Based on an analysis of 89 prospective and case-control studies, exposure to bug or weed killers and solvents increased the risk of developing Parkinson’s disease by 33% to 80%, reported Gianni Pezzoli, MD, of the Parkinson Institute, Istituti Clinici di Perfezionamento in Milan, and Emanuele Cereda, MD, PhD, IRCCS University Hospital San Matteo Foundation in Pavia, Italy.
However, the evidence remains “limited, or at least inconclusive,” because of lack of definitive agreement between cohort and case-control studies, the authors cautioned in the May 28 issue of Neurology.
The investigators examined research that considered pesticides, herbicides, insecticides, fungicides, rodenticides, solvents, organochlorines, organophosphates, paraquat, maneb/mancozeb, and DDT, for their relations to Parkinson’s disease.
They also looked at proximity to exposure, such as farming, well-water for drinking, and rural living. The relative risk for Parkinson’s in relation to agricultural jobs was 1.33 (95% CI 1.14-1.56,P<0.001), they stated. Sensitivity analyses based on more than 100 incident cases, they wrote, “confirmed the risk associated with agriculture jobs.”
Paraquat showed a two-fold increase in risk for Parkinson’s, but no association was found to DDT, the authors wrote.
But due to heterogeneity, the results were conflicting. For instance, higher quality studies showed statistical significance for the exposure to solvents, paraquat, and well-water drinking, but they also showed a reduction in risk of Parkinson’s, specifically in relation to insecticides, farming, and well-water drinking. However, high quality studies showed an increase in risk for Parkinson’s for exposure to solvents of more than 30%.
In sensitivity analyses on high-quality studies of more than 200 cases, the risks of Parkinson’s related only to rural living became significant (1.51, 95% CI 1.13-2.03, P=0.006).
The authors offered some explanations for their results. First, heterogeneity in case-control studies seemed to relate mainly to study quality and size, and they had to rely on these data rather than preferred cohort studies to determine etiologic relationships.
In addition, in prospective studies, differences in estimates of exposure to pesticides appeared to depend on the method of ascertainment of Parkinson’s disease, they said.
A study limitation was that the authors did not assess the effect of any secondary causes of Parkinson’s disease in patients recruited from movement disorders clinics.
Nonetheless, “I think the study is actually a big advance in our research knowledge of the relation between chemical exposures and the basic neurological injuries,” said Arch Carson, MD, PhD, of the University of Texas School of Public Health in Houston. “This report is the first to show that there is a positive relationship between not only insecticides and herbicides but also some other solvent chemicals to which many people are exposed and the development of Parkinson’s syndrome.”
But Carson also pointed that the research had clinical limitations. “It does not provide us in medical practice any clear pathway for the treatment of Parkinson’s disease, or even its prevention,” he explained. “We do know there is a significant relationship between various chemical exposures and the development of Parkinson’s disease, as well as a significant relationship with things like family history, smoking, and occupation … but it’s very difficult to put these things into practice except in terms of preventive health, and reducing or eliminating exposures to such suspect materials over time.”
The authors called for more research as did Carson, looking for information on the “specific … and mechanistic relationships between chemical exposure and neurologic injury.”
“We’re only starting to open that black box and understand the details of how that works chemically within the human body, but we’re making progress very fast,” he said. “This study is a benchmark in that process.”