In Reply The interest of Martins and Carruthers regarding our study on pesticide levels and Alzheimer disease1 is appreciated. The primary tenet of their letter relates to the hypothesis that the mechanism by which pesticide exposure may contribute to Alzheimer and Parkinson diseases is through an antitestosterone effect. This hypothesis appears to be based on several cited review articles suggesting that androgens may play a role in cognitive aging and in the etiology of Alzheimer disease. Furthermore, Martins and Carruthers cite an article from 20 years ago regarding the antiandrogenenic effects of dichlorodiphenyldichloroethylene (DDE).2 On close inspection of the article, the dose or levels of DDE required to produce modest effects on androgen receptor binding and antiandrogenic effects are orders of magnitude higher than the serum levels we observed in our study and much higher than those observed in studies of highly exposed populations. Additionally, recent studies reported that populations highly exposed to dichlorodiphenyltrichloroethane/DDE3,4 or men aged 18 to 51 years in the United States5 either have no change or slightly increased levels of testosterone. Thus, although testosterone deficiency may well contribute to cognitive deficits and perhaps Alzheimer disease, the likelihood it contributes to the relationship between DDE and Alzheimer disease is exceedingly small. However, future studies are required to conclusively rule out an association between DDE levels, low testosterone, and Alzheimer disease. In our prior studies, we found no relationship between DDE and Parkinson disease.6,7
Richardson JR. Testosterone as the Missing Link Between Pesticides, Alzheimer Disease, and Parkinson Disease—Reply. JAMA Neurol. 2014;71(9):1190. doi:10.1001/jamaneurol.2014.1814
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