Since I’ve started working on this project, many people have asked me if Parkinson’s disease is “genetic or environmental”. One of the most frequently cited studies on this question looked at twin brothers: identical twins versus fraternal twins. If one twin got Parkinson’s, would the other twin get it as well?
If Parkinson’s was genetic, we would expect both identical twin brothers to get Parkinson’s more often than both fraternal twin brothers. Why is this? Because identical twins share much more genetic information than fraternal twins, who share as much genetic information as regular brothers. More genetic information means more likelihood that both identical twins will share traits, including disease risk, that are caused or influenced by heritable factors.
So what did the study find? The study found that Parkinson’s occurred more frequently in the other identical twin brother only if the age of disease onset was 50 or earlier. In other words, Parkinson’s is more likely to be “genetic” when the disease begins before age 51.
The study was done back in 1999 by The Parkinson’s Institute and published in the Journal of the American Medical Association. Here’s the study abstract: http://www.ncbi.nlm.nih.gov/pubmed/9929087
But there are a few weaknesses of the study and its conclusion.
- In order to better examine the influence of a shared childhood environment, the researchers could have studied identical twins or other siblings raised separately or adopted children raised together, where at least one sibling has Parkinson’s. The study assumes that similarity between twins is genetic, whereas some of it may be due to shared upbringing (environmental factors).
- We know that mitochondria are of critical importance to Parkinson’s disease, yet mitochondria are not inherited via the traditional Mendelian pattern. The study assumes the Mendelian pattern of nuclear genetics, so the conclusions are less clear.
- Age of onset can be very different even for identical twins with a known mutation that causes Parkinson’s. Therefore, if one twin has Parkinson’s, but the other twin doesn’t – this doesn’t mean that the other twin won’t eventually get it as well. The age variance makes this kind of research very challenging. For more on Parkinson’s age variation, see: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3664414/
Nonetheless, these results suggest that research is best focused on environmental factors, including environmental toxins and traumas, or insufficient exposure to neuroprotective factors in the diet or elsewhere. Genetic factors may be informative in terms of understanding the various pathways to a Parkinson’s diagnosis, but the information is not directly applicable to the vast majority of sufferers and their families.
So is Parkinson’s environmental then? Not exactly. More and more research is emerging, suggesting that environmental-genetic interactions contribute more to Parkinson’s disease than do genetic factors or environmental factors alone. For those that would like to see some examples of such interactions, read this review: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3454809/
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