Genetics & Chemicals – With Comments from Dr. Gordon
By Linda on Jan 28, 2011 in F.I.G.H.T. | comments(0)
Genetics also influences our ability to withstand the chemicals we are exposed to, as in this research on Parkinson’s disease. Remember some can eat fish and the mercury they consume clears in as little as 40 days whereas others take nearly 6 months to clear the same dose of mercury.
It might be best to at least do something every day from early childhood on such as extra C or EDD (Essential Daily Defense), which I suggest to start before age 1. Okay to use one cap per 20 # weight and 1 Gm of BioEn’R-G’y C (1/4 tsp) per 10 pound of weight or per 1 year of age during the entire lifespan.
We have proof from Harvard that the lower level of lead in bones reduces dramatically the incidence of death from heart disease (i.e. high levels have 6 times the death rate) so this is a life time challenge we all face now that we have polluted our earth.
President, Gordon Research Institute
www.gordonresearch.com
From the aDepartment of Epidemiology, UCLA School of Public Health, Los Angeles, CA; bDepartment of Environmental Health Sciences, School of Public Health, UC Berkeley, CA; cDepartment of Preventive Medicine, Keck School of Medicine, University of Southern California, Los Angeles, CA; dDepartment of Neurology, UCLA School of Medicine, Los Angeles, CA; and eDepartment of Environmental Health Sciences, Center for Occupational and Environmental Health (COEH), UCLA School of Public Health, Los Angeles, CA.BACKGROUND:: Human, animal and cell models support a role for pesticides in the etiology of Parkinson disease. Susceptibility to pesticides may be modified by genetic variants of xenobiotic enzymes, such as paraoxonase, that play a role in metabolizing some organophosphates.
METHODS:: We examined associations between Parkinson disease and the organophosphates diazinon, chlorpyrifos, and parathion, and the influence of a functional polymorphism at position 55 in the coding region of the PON1 gene (PON1-55). From 1 January 2001 through 1 January 2008, we recruited 351 incident cases and 363 controls from 3 rural California counties in a population-based case-control study. Participants provided a DNA sample, and residential exposure to organophosphates was determined from pesticide usage reports and a geographic information system (GIS) approach. We assessed the main effects of both genes and pesticides in unconditional logistic regression analyses, and evaluated the effect of carrying a PON1-55 MM variant on estimates of effects for diazinon, chlorpyrifos, and parathion exposures.
RESULTS:: Carriers of the variant MM PON1-55 genotype exposed to organophosphates exhibited a greater than 2-fold increase in Parkinson disease risk compared with persons who had the wildtype or heterozygous genotype and no exposure (for diazinon, odds ratio = 2.2 [95% confidence interval = 1.1-4.5]; for chlorpyrifos, 2.6 [1.3-5.4]). The effect estimate for chlorpyrifos, was more pronounced in younger-onset cases and controls (</=60 years) (5.3 [1.7-16]). No increase in risk was noted for parathion.
CONCLUSION:: The increase in risk we observed among PON1-55 variant carriers for specific organophosphates metabolized by PON1 underscores the importance of considering susceptibility factors when studying environmental exposures in Parkinson disease.
