Genes can make brains vulnerable
15 August 2013. For simplicity, brain researchers often assume that we are all almost equally sensitive to toxic compounds. So we calculate average risks of brain drain effects and anticipate that nobody is more than 10 times as sensitive. Although this assumption is commonly made by regulatory agencies, we suspect that much greater susceptibility does occur. But there has been scattered documentation only – until now.
Researchers in the US wondered why some people seemed to suffer neurological symptoms related to their amalgam fillings, while others were not bothered. Could it be that some people were more sensitive to the tiny traces of mercury released from the tooth restorations, but others not?
In a study of dentists and dental assistants, deficits in neuropsychological performance occurred most frequently if the subject had a mutation of a metabolic gene, and increased frequency of symptoms occurred in those who had mutations in a gene that codes for an important brain enzyme. A new report shows that mutations in the gene responsible for formation of metal-binding metallothionein may make children more susceptible to adverse effects from mercury amalgams. These studies clearly suggest that we are not all equally sensitive to mercury vapor.
Other new research suggests that gene mutations may also determine whether we are vulnerable to methylmercury from fish and seafood. Mutations exist in genes that control the organic molecule called glutathione, which affects the fate of mercury in the body, and retention of methylmercury appears to depend on these mutations, as shown in a new study from the Brazilian Amazon.
This evidence has now been extended in a study of children who were born in the United Kingdom 20 years ago. Scanning the relevant genes that could be relevant to mercury brain drain, the research group (in which PG participated) found four genes, where one or two mutations at a particular location was associated with a much greater mercury-associated loss in the IQ that was measured at age 8 years. Children without the mutations appeared to be virtually resistant to prenatal methylmercury exposure. The results were presented at a conference earlier this month.
These findings have two important implications. First, when we conduct risk assessments for chemical brain drainers, we are making a serious error assuming that sensitivity varies only little. If exposure limits are based on the average sensitivity, a substantial proportion of the population may not be protected. For example, the European Food Safety Authority recently decided that the most vulnerable children are no more than 2-fold as sensitive as the average. The new research shows that this assumption is way too optimistic and puts many children in danger.
Second, genetic factors play a crucial role in brain development, but genes alone cannot explain recent increases in the reported prevalence of neurodevelopmental diseases. Also, none of the genes discovered so far appears to be responsible for more than a very small percentage of the cases. In total, genetic factors may account for no more than about 30-40% of all cases of neurodevelopmental disorders. Thus, non-genetic, environmental exposures must be involved in the causation. The new research suggests that brain drainers may interact with mutations in specific genes. Future studies therefore need to take into account that average brain toxicity may sometimes appear to be small, but that vulnerable subgroups may carry the brunt of the damage.