PLOS Article on Climate, Genes and Metabolic Disorders

Metabolic disorders relate to how the body absorbs food and processes into energy. Diabetes is an example of a metabolic disorder. Here are some stats on diabetes from the World Health Organization:

Diabetes is a chronic disease that occurs when the pancreas does not produce enough insulin, or alternatively, when the body cannot effectively use the insulin it produces. Insulin is a hormone that regulates blood sugar. Hyperglycaemia, or raised blood sugar, is a common effect of uncontrolled diabetes and over time leads to serious damage to many of the body's systems, especially the nerves and blood vessels.

The World Health Organization (WHO) estimates that more than 180 million people worldwide have diabetes. This number is likely to more than double by 2030.
In 2005, an estimated 1.1 million people died from diabetes.

Almost 80% of diabetes deaths occur in low and middle-income countries. Almost half of diabetes deaths occur in people under the age of 70 years; 55% of diabetes deaths are in women.

WHO projects that diabetes deaths will increase by more than 50% in the next 10 years without urgent action. Most notably, diabetes deaths are projected to increase by over 80% in upper-middle income countries between 2006 and 2015.

Prevention of type 2 diabetes can be achieved by maintaining a healthy weight and exercising.

Like my previous post on Why We Develop Cancer, one can ask why we, as a species, develop metabolic disorders? The latest issue of PLOS Genetics has a very interesting study which examines this question. And the study's conclusions are truly fascinating-- adaptations to climate might be an important part of the story.

The article is entitled "Adaptations to Climate in Candidate Genes for Common Metabolic Disorders" by Angela Hancock et. al. and you can download it for free here. Here is a summary of their findings:

The human species inhabits a wide geographical range encompassing a diversity of climates, and adaptation to these climates likely played an important role in shaping genetic and phenotypic variation among populations. We hypothesized that spatially varying selective pressures related to climate shaped the frequencies of genetic variants in the energy metabolic pathway. To test this hypothesis, we examined patterns of genetic variation in 82 candidate genes for common metabolic disorders across the 52 globally dispersed populations of the Human Genome Diversity Project. We applied a combination of statistical approaches to test whether the geographic distribution of these variants could be accounted for by differing climates, consistent with a signal of spatially varying positive selection. For several climate variables, we observed signals in excess of that expected from human population history and chance alone. Significantly, many of these signals were from genes previously shown to affect cold tolerance and disease risk. Our results provide evidence that variation among human populations in susceptibility to common metabolic diseases may be due, in part, to different histories of selective pressures on genes in these disease pathways. Furthermore, our results point to additional genes and variants that are suitable targets for follow-up disease association studies.

Cheers,
Colin