This surprising finding is presented by American, Swedish, and Dutch scientists in a study being published today in the prestigious journal American Journal of Human Genetics. The finding may be of great significance for research on hereditary diseases and for the development of new diagnostic methods.
How can it be that one identical twin might develop Parkinson's disease, for instance, but not the other" Until now, the reasons have been sought in environmental factors. The current study complicates the picture.
Even though the genome is virtually identical in identical twins, our results show that there in fact are tiny differences and that they are relatively common. This could have a major impact on our understanding of genetically determined disorders, says Jan Dumanksi, who co-directed the international study with his colleague Carl Bruder.
By uncovering these small genetic differences in identical twins where one of them is sick, we have a way of tying specific genetic changes to the genesis of common diseases, says Carl Bruder.
These researchers studied 19 pairs of identical twins and found that they indeed had the same DNA but nevertheless evinced differences in the number of copies of individual DNA segments. A segment might be missing, or more copies might exist in one twin. This could explain how one identical twin can be afflicted with a disorder while the other twin remains fully healthy, according to the scientists.
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Other genes that varied according to climate included several involved in heat production, cholesterol metabolism, energy use, and blood glucose regulation. Not all cold-tolerance-related gene variants protect against metabolic syndrome. Increased blood glucose levels, for example, could protect someone from the cold by making fuel more readily available for heat production, yet it raises the risk of type 2 diabetes. The version of a gene known as FABP2 that became more common as temperatures fell causes increased BMI, promotes fat storage and elevates cholesterol levels. This would protect against the cold, but increase susceptibility to heart disease and diabetes.
"All these genes are likely to be involved in metabolic adaptations to cold climates," said Di Rienzo, "but they have opposing effects on metabolic syndrome risk. We suspect they spread rapidly as populations settled into colder and colder climates at higher latitudes, but in the modern era they have taken on a whole new significance, as the supply of calories from food has mushroomed and the survival advantage of generating more heat has been minimized by technology."
The authors suggest that the search for genes that vary according to climate could provide additional clues about the onset of metabolism related diseases.
"The biological processes that influence tolerance to climatic extremes," the authors conclude, "are likely to play important roles in the pathogenesis of common metabolic disorders Our results argue for a role of climate adaptations in the biological processes underlying the metabolic syndrome and its phenotypes."
This work was funded by The National Institutes of Health. Additional authors include Angela Hancock, David Witonsky, Adam Gordon, Gidon Eshel, Jonathan Pritchard and Graham Coop of the University of Chicago.
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