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01-05-2013, 12:30 AM | #1 | |||
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Researchers demonstrate the link between pesticides and Parkinson’s disease
Although it was assumed for many years that between Parkinson’s disease and pesticides is a link, only now neuroscientists at UCLA have been able to demonstrate this connection. They knew that some common chemicals in Central California, such as paraquat, maneb and ziram, increase the risk of Parkinson’s disease, and this was observed not only in farmers, but also in residents of the area who have inhaled these particles. Now investigators at UCLA have made another discovery: it seems that Parkinson’s disease is related to a fourth chemical, a substance called benomyl, whose effects persist even after 10 years. ... it seems that the harmful effects triggered by benomyl occur even in people who have Parkinson’s but have not been exposed to pesticides. ...benomyl triggers a series of events leading to Parkinson’s disease onset. It is assumed that the chemical interferes with an enzyme called ALDH (aldehyde dehydrogenase). In this way, aldehyde dehydrogenase can not prevent accumulation of DOPAL, a toxic substance that has harmful effect on neurons and which greatly increases the risk of developing Parkinson’s disease. Benomyl is a substance that has been widely used in the U.S. until it was banned in 2001 because it was found to have toxic effects on health... the destructive effect of benomyl on dopaminergic neurons has been shown in cell culture experiments. Now neuroscientists at UCLA believe that this cascade of events occurs in all patients with Parkinson’s disease. If they were create a drug to protect aldehyde dehydrogenase enzyme activity, they could treat or prevent Parkinson’s disease... As stated the study’s first author, Arthur G. Fitzmaurice, a postdoctoral scholar in Bronstein’s laboratory, only a small fraction of cases of Parkinson’s are due to heredity. Therefore, environmental factors have an important role. Read more: http://www.doctortipster.com/12452-r...#ixzz2H4ljM1sy
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In the last analysis, we see only what we are ready to see, what we have been taught to see. We eliminate and ignore everything that is not a part of our prejudices. ~ Jean-Martin Charcot The future is already here — it's just not very evenly distributed. William Gibson |
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01-05-2013, 11:30 AM | #2 | |||
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Junior Member
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This is an exciting finding. It might help to explain why there is such a high incidence of PD in the Amish community. Try as researcher's may, they've been unable to find a hereditary link to date.
Like many, I've been exposed to pesticides on the farm and chemicals in the laboratory. My mother was a heavy smoker during her pregnancy. I've wondered if my father's exposure to the Bikini Atoll atom bomb tests affected the development of my central nervous system. My personal opinion is that PD is the combined damage caused by many small factors. It's nice to see that science is finally starting to get a handle on what some of those factors really are. Steve |
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01-05-2013, 01:29 PM | #3 | |||
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In Remembrance
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The explanation that this group offers is dependent on geography. By that I mean that it assumes that a geographically limited variable (i.e. use of this pesticide in that valley) explains everything. Unfortunately, this would produce clusters downwind of agriculture that would have JohnT's maps lit up like Christmas trees and that just is not the case. I suspect that this study is another of those "more study is needed until I get tenure" types.
As for the Amish, the inflammation hypothesis handles that easily. Theirs is a horse powered existence and they use a lot of hay. Dusty hay that goes deep into the lungs when inhaled and ups the inflammatory ante. And there is also the fact that the Amish rely on kerosine lamps. The hydrocarbon soot is extremely small nanoparticles and, again, penetration is deep. -Rick
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Born in 1953, 1st symptoms and misdiagnosed as essential tremor in 1992. Dx with PD in 2000. Currently (2011) taking 200/50 Sinemet CR 8 times a day + 10/100 Sinemet 3 times a day. Functional 90% of waking day but fragile. Failure at exercise but still trying. Constantly experimenting. Beta blocker and ACE inhibitor at present. Currently (01/2013) taking ldopa/carbadopa 200/50 CR six times a day + 10/100 form 3 times daily. Functional 90% of day. Update 04/2013: L/C 200/50 8x; Beta Blocker; ACE Inhib; Ginger; Turmeric; Creatine; Magnesium; Potassium. Doing well. |
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01-08-2013, 12:26 AM | #4 | |||
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Senior Member
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In the last analysis, we see only what we are ready to see, what we have been taught to see. We eliminate and ignore everything that is not a part of our prejudices. ~ Jean-Martin Charcot The future is already here — it's just not very evenly distributed. William Gibson |
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"Thanks for this!" says: | mudfud27 (01-10-2013) |
01-10-2013, 06:11 PM | #5 | ||
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Junior Member
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Quote:
The explanation that we offer is that inhibition of aldehyde dehydrogenase, (or one of the other enzymes involved in detoxifying dopamine metabolites, but we really focused on ALDH here) can be a contributor to the pathogenesis of PD. Importantly, it sheds light on one of the greatest mysteries of PD, which is the semiselective vulnerability of dopaminergic neurons-- an issue which is extremely poorly understood. Moreover, it suggests an entirely new avenue of attack in developing disease modifying therapies that was previously unexplored. We were able to identify this because of the pesticide exposure, but that does not mean that ONLY this pesticide could cause this type of inhibition-- there are several potential mechanisms including genetics and various other exposures. In no way is our explanation restricted by geography, nor do we claim it explains "everything". Nevertheless, you ought to rethink your "maps" comment since there certainly are PD clusters in agricultural areas. I hope this clears up some of your misconceptions. |
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"Thanks for this!" says: | Lemonlime (01-10-2013), soccertese (01-10-2013) |
01-14-2013, 02:38 AM | #6 | ||
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Senior Member
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This thread appears to be based on a paper by Fitzmaurice et al. [1]. Unfortunately this is behind a pay wall. The paper's abstract, however, is available. In it the authors propose:
"that benomyl, via its bioactivated thiocarbamate sulfoxide metabolite, inhibits aldehyde dehydrogenase (ALDH), leading to accumulation of the reactive dopamine metabolite 3,4-dihydroxyphenylacetaldehyde (DOPAL), preferential degeneration of dopaminergic neurons, and development of PD." So, the claim, as I understand it, is that, at least in part, PD is caused by the inhibition of ALDH. This suggests to me that further work is needed to see whether this could lead to possible therapies based on alcohol and tea. Chrostek et al. write [2]: "Chronic ethanol consumption significantly increased the liver ALDH activity in young and adult rats but decreased this activity in old animals. The drinking of green tea did not alter ALDH activity in ethanol-consuming rats. Drinking green tea alone significantly increased ALDH activity in young and adult rats but did not alter this activity in old rats." I can't find a clear picture of the relationship between PD and alcohol, but a feature article in Neurology Review [3] says: "People who moderately consume beer may reduce their risk of developing Parkinson’s disease by 27%, compared with nondrinkers." The picture with green tea is also unclear, but Quintana [4] states: "There was a clear protective effect of tea consumption in the pooled risk estimate [OR: 0.83 (95% confidence interval 0.74 to 0.92)] with 2215 cases and 145578 controls." In writing this post I came across a thread [5] from two years ago started by cockankat, to whom my thanks, that reports on the relationship between ALDH and DOPAL and reports that "analysis of 14 brains of people who died with Parkinson disease had 4.4 times more DOPAL than the brains of people without Parkinson disease" and that ALDH is deficient in PwP. References [1] "Aldehyde dehydrogenase inhibition as a pathogenic mechanism in Parkinson disease" Arthur G. Fitzmaurice, Shannon L. Rhodes, Aaron Lulla, Niall P. Murphy, Hoa A. Lam, Kelley C. O’Donnell, Lisa Barnhill, John E. Casida, Myles Cockburn, Alvaro Sagasti, Mark C. Stahl, Nigel T. Maidment, Beate Ritz, Jeff M. Bronstein PNAS, vol 110, no 2. http://www.pnas.org/content/110/2/636.abstract [2] "The effect of green tea on the activity of aldehyde dehydrogenase (ALDH) in the liver of rats during chronic ethanol consumption." Chrostek L, Tomaszewski W, Szmitkowski M. Rocz Akad Med Bialymst. 2005;50:220-3. http://www.ncbi.nlm.nih.gov/pubmed/16358971 [3] "Does Alcohol Consumption Reduce the Risk of Parkinson’s Disease?" Neurology Reviews 2011;19(12)14-15. http://www.neurologyreviews.com/Arti...SI=&FullText=1 [4] "Parkinson's Disease and Tea: A Quantitative Review" José Luis Barranco Quintana, MD, MPH, Mohamed Farouk Allam, MPH, PhD, Amparo Serrano Del Castillo, MD, PhD and Rafael Fernández-Crehuet Navajas, MD, PhD J Am Coll Nutr February 2009 vol. 28 no. 1 1-6 http://www.jacn.org/content/28/1/1.full [5] http://neurotalk.psychcentral.com/sh...highlight=aldh John
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Born 1955. Diagnosed PD 2005. Meds 2010-Nov 2016: Stalevo(75 mg) x 4, ropinirole xl 16 mg, rasagiline 1 mg Current meds: Stalevo(75 mg) x 5, ropinirole xl 8 mg, rasagiline 1 mg |
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"Thanks for this!" says: | Conductor71 (01-15-2013) |
01-16-2013, 11:24 AM | #7 | |||
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I react very quickly to the chemicals road crews spray along the sides of the road to kill weeds. I also feel very bad when I have worked with dusty hay. It is interesting to me that I can react so quickly to some chemical or paint that my dad is using (who is 87) he seems un-effected by the fumes and I have to "run for my life" to get away from them
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