ADHD in Children Linked to Pesticide Exposure in Mothers
Researchers from the University of Michigan School of Public Health have determined that pesticide exposure in mothers is linked to Attention Deficit Hyperactivity Disorder in their children.
The researchers tested a large population of children and their mothers from Mexico City. The researchers analyzed their DNA and correlating the DNA data with the children’s ADHD levels.
Of the population, 989 mothers tested positive for the expression of one of two pesticide enzymes called paraoxonase-1, and 1,010 children tested positive for paraoxonase-1.
When a person is exposed to a significant amount of pesticides, the body will produce an enzyme called paraoxonase-1. This enzyme will break down the pesticide into smaller components to be escorted out of the body—or assumed by fat cells.
Because the production of this enzyme is expressed by the DNA – the DNA will reveal which mothers and children have been exposed to a significant amount of pesticide residue.
The researchers then correlated ADHD scores from the non-paraoxonase-1 mothers and children and compared them with the ADHD scores of those without paraoxonase-1 expression.
The researchers found that children of mothers with paraoxonase-1 DNA expression (PON1) had an average of 2.17 points higher on the DSM IV Hyperactivity/Impulsivity scores, and 2.27 higher scores on the DSM IV Child Attention problems.
However, the PON1 DNA marker in children but not mothers was unrelated to higher Attention Deficit Hyperactivity Disorder scores in the children.
This illustrates that the tendency for ADHD is increased significantly when the parent has significant pesticide exposure at some point, which has an effect upon their genes.
Epigenetic relationship with pesticides
This science of genetic changes from environmental inputs is called epigenetics. As we are exposed to certain environments and our bodies respond physiologically, our genes will reflect that response. And unfortunately in this case, that genetic change will be passed on to the children. One of the classic studies of epigenetics is the study of famines in years past and how those famines will be reflected in the genes of generations after.
But in the case of pesticide exposure, we can see that what is passed along reflects the nervous system of the child.
Direct child exposure also influences learning and behavior
This doesn’t mean that pesticide exposure doesn’t effect a child’s learning or cognition. An Egyptian study of 50 children who worked in fields and applied pesticides were tested against children not exposed.
The study found that the exposed children performed much worse on neurobehavioral testing compared to those not exposed.
Many pesticides are neurotoxins
This is only logical because many pesticides are actually neurotoxins.
This was confirmed in a Harvard School of Public Health study of 143,325 people. The study found that 7,864 people had significant pesticide exposure, including farmers, fishermen and ranchers.
The research found that those exposed to pesticides had a 70% higher incidence of Parkinson’s disease than those who were not exposed to pesticides.
Furthermore a French study of farmers found that pesticide exposure significantly reduced cognition scores among those. Pesticide exposure resulted in low scores at a risk of up to five times, while the risk of a two-point drop in Mini-mental State Examination scores was more than double among those with pesticide exposure.
What to do?
The question now becomes: When will our society stop poisoning our bodies and our children’s bodies? What more do we need to learn before we make the appropriate changes?
Better yet, when we will decide that our health and the health of our pesticides is more important than the convenience of using neurotoxic pesticides?
There are many natural and/or nontoxic pesticides that can be applied in and around our homes. Some kill pests and others repel them. An internet search for “natural pesticides” will reveal many choices.
An organic diet will also reduce pesticide exposure.
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