Findings from a recent study identifies why individuals from developing countries are at a greater risk for obesity and type 2 diabetes than those in the West.
The incidence of metabolic disorders particularly affects individuals in developing countries, as access to food becomes more readily available and subsequently results in greater overall caloric intake. The middle classes of developing countries are thus at a greater risk for developing type 2 diabetes and cardiovascular disease due to obesity than those in the West. As a result, it is projected that individuals from developing countries will face more than 70% of the global burden of type 2 diabetes by 2030.
While it has been commonly accepted that higher caloric intake contributes to the onset of type 2 diabetes, there has been a gap in research to account for why a ‘normal’ diet can contribute to obesity and its associated morbidities. Recent findings published in Cell Metabolism points to the role that epigenetics, where environmental factors influence the expression of certain genes, plays in such outcomes.
The latest findings highlight that undernourishment of our ancestors is an important factor to consider, especially as they pertain to the concept of feast vs. famine. The concept of feast vs. famine states that during times of abundance, the body will store excess nutrients for when there is a scarcity of food availability, such as a famine, and rely on them in order to survive.
The researchers at the University of Sydney simulated a 12-year study consisting of two groups of rats, whereby one group was undernourished for 50 generations and then provided a normal diet two generations afterwards; the second group maintained a normal diet for 52 generations. The first scenario would be typical of populations where ancestors were deprived of food availability but later had such conditions reversed, as witnessed in developing countries.
At the end of the study the descendants from the first scenario were 8 times more susceptible to develop type 2 diabetes than the rats that were fed a normal diet for 52 generations during the 12-year period. The reasoning behind such findings relate to the function of epigenetics and their role in evolution. More specifically, populations in which their ancestors experienced undernourishment (or famine) did not experience changes in their epigenetic makeup. This means that the descendants of ancestors that were undernourished did not adapt to the dietary changes of their diets, but rather still were programmed to deal with conditions of undernourishment.
Despite new environmental conditions, the epigenetic expression of populations no longer facing the same environmental conditions as their ancestors was not modified. Consequently, these descendants were more likely to store fat and handle the dietary changes in way that predisposed them to a greater likelihood of obesity and its metabolic effects on the body in comparison to populations that experienced normal diets multi-generationally. In essence, the function of obesity would have been to help previously nutrient-deprived individuals have a store of nutrients from which their bodies could draw from in times of food deprivation.
While the results from the study did not account for why new environmental conditions did not influence an alternate expression of genes, the findings do lend support to the notion that evolution and gene expression are a slow multi-generational process.
The findings are relevant to today’s world because of the accessibility of highly processed foods in countries that were previously undernourished and the migration of populations from developing countries to more affluent ones. Individuals from such populations are more likely to be at-risk for metabolic diseases associated with obesity, which can be traced to the living conditions of their ancestors. By identifying the contributing factors that result from undernourishment to sudden over-nourishment, incidences of metabolic disorders can be better understood and mitigated for future generations.