Scientists from the Stanford School of Medicine in the US have been researching whether the human race may have evolved to be more susceptible to type 1 diabetes.
The findings are published online in the journal Public Library of Science ONE.
They say that gene variants that lead to conditions such as type 1 diabetes and rheumatoid arthritis have other advantages which may have prevented them being destroyed by the process of natural selection.
The researchers speculate that this evolutionary change may have happened to protect carriers against certain diseases, a throw back to the past when most infectious diseases were untreatable.
In some diseases such as sickle cell anaemia, a gene variant, when present in two cases, makes the individual develop the condition. Although it seems logical that nature would work to eliminate the disorder eventually, the variant is common in some parts of Africa and a single copy of the variant means that an individual is less susceptible to developing another infectious disease, malaria.
In the study, the scientists looked at specific locations in DNA called SNPs (single nucleotide polymorphisms) in relation to type 1 diabetes and type 2 diabetes, rheumatoid arthritis, hypertension, Crohn’s Disease, coronary artery disease and bipolar disorder. Some SNPs are associated with increased risk of developing disease and some SNPs offer an immunity against some diseases.
In relation to type 1 diabetes, the researchers found that of the top SNPs associated with the condition, 80 have been recently increasing in prevalence, meaning that they have undergone positive selection. Of these, 58 were found to be associated with an increased risk of the disorder, while 22 were found to be protective.
It was a similar story with rheumatoid arthritis. Interestingly, the scientists found that we are evolving away from Crohn’s Disease - more protective SNPs were found as opposed to risk inducing ones for this condition.
The results for type 2 diabetes, coronary heart disease and bipolar disorder showed that protective and risk inducing SNPs were present in equal measures.
The researchers believe that in some areas of the world where triggers for some of these complex diseases exist to a lesser degree, carriers might only experience the protective effect against some types of infectious disease.
The investigation is now being expanded to take into account more SNPs and diseases.