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ShareDec. 26, 2006 — Research published in the Journal of Epidemiology and Community Health casts doubt on the belief that organophosphate poisoning causes symptoms of depression among Gulf War veterans and farmers, who are exposed regularly to these chemicals.
Several previous studies have found that people who are regularly exposed to organophosphates are more likely than the general population to have symptoms of depression, including irritability, difficulty concentrating and poor sleep patterns.
But these studies do not prove that organophosphates are responsible for these symptoms.
In a bid to look at the association more closely, researchers from the University of Bristol tested out the theory among older women between the ages of 60 and 79, who would not have been habitually exposed to organophosphates in the course of their employment.
The women were already part of a long term study of women's health, involving more than 4,000 participants from 23 British towns.
They were surveyed about their levels of depression, and blood samples were taken for genetic testing.
Because an individual’s genetic make-up (genotype) is randomly determined from their parents’ genotype at the time of conception, genes can be used to test whether a non-genetic factor (for example, organophosphates) causes a disease.
The PON1 Q192R gene comes in three versions (QQ, QR or RR) and individuals with the RR version tend to metabolise organophosphates more slowly than those with either of the other versions.
Several previous studies have shown that Gulf War Veterans and sheep dippers with the RR genotype had a higher probability of symptoms.
In agreement with this, the results from the new study found that women in the study with the genetic variant were significantly more likely to report depression than those without the variant.
But because these women had not been exposed to organophosphates, these new findings suggest that the association of this gene with depressive symptoms is unlikely to be explained by organophosphate poisoning, because the association is the same, irrespective of exposure to organophosphates.
In fact, the authors suggest that exposure to more mundane everyday toxins or activities, rather than the specific chemical hazards found in warfare and farming, are likely to have a role.
The authors also note that recent research has suggested that rather than slowing the capacity to clear organophosphates from the body, the genetic variant actually does the opposite and speeds it up, so minimising exposure.
The authors point out that their findings do not negate the biological basis theory of the Gulf War Syndrome, but suggest that reliance on genetic vulnerability studies in specific groups is 'perhaps misplaced'.
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