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Our early human ancestors originated from a hot, humid climate where natural selection focused on dispersing heat. As humans migrated to colder climates there would have been evolutionary pressure to adapt to their new settings by boosting the processes that produce and retain heat.
Genes involved in energy metabolism are therefore likely to be central to heat and cold tolerance.
Researchers from the Dept of Human Genetics, University of Chicago, USA tested this theory by genotyping 873 tag SNPs in these ‘cold tolerance’ genes in 54 worldwide populations and found a correlation with climatic variations.
Among the results were strongest signals from several SNPs, that had previously been associated with body evolution directly related to cold tolerance.
One, a leptin receptor, LEPR R109K, which is integral in appetite regulation and energy balance, was the source of one of the strongest signals of evolutionary selection. One version of this gene is common in locations with colder winters. This allele is additionally correlated with the increased capability to absorb oxygen and expel carbon dioxide, which happens when the body produces heat. The same genetic variation has also been linked to a lower BMI, a smaller amount of abdominal fat, and a lower blood pressure. This specific leptin receptor, therefore, is protective against metabolic syndrome.
However, not all of the genes related to tolerance of colder climates protects against the metabolic syndrome. For example, an increased blood glucose level might protect the body from cold weather by making energy more readily available for production of heat. However, this also raises the risk of type 2 diabetes. FABP2 A54T was a gene that was more prevalent in populations with lower temperatures actually increases BMA, promotes storage of fat in the body and increases levels of cholesterol. While this protects the body against the cold, it increases the risk of heart disease and diabetes, and thus metabolic syndrome.
Variation in climate may be correlated with other aspects of environmental variation. Nevertheless, the results are consistent with the idea that climate has been an important selective pressure acting on candidate genes for common metabolic disorders such as obesity, diabetes and heart disease.
Thousands of years later we live in an era that combines widespread central heating with an overabundant food supply, so those genetic alterations which protected us from cold have taken on a different sort of significance. They alter our susceptibility to a whole new set of diseases, such as obesity, coronary artery disease and type 2 diabetes.
For further information, please click on:
Elaine Warburton www.geneticsandhealth.com
