Epigenetics: A Thrifty way of using DNA

By Kim Meyers, Class of 2016

Most of us strive to lead healthy and happy lives. But our vulnerability to disease in adult life can be shaped long before we even leave the womb.

Photo credit - Caroline Davis2010
Image Credit – Caroline Davis2010 via Flicker

Life is incredible. Strands of DNA drive our development and allow us to transform from a single cell, to a freaky looking bean before becoming functioning human beings. Or some other animal, depending on your species. But the fact is before we’re even born, before we can take our first breath, countless factors are trying to change us.


DNA is often referred to as the instructions in a cell, which can carry out various functions, create certain substances or signal other cells. But the way these instructions are read can be altered so that the outcome changes without needing changes to the DNA sequence itself. This is called epigenetics and is amazing because changes that occur while in the womb can have an effect on our survival later in life. But what if these changes are not beneficial? Could they make us more vulnerable to disease later in life? Imagine this:

It’s September, 1944 and the Western Netherlands are feeling the effects of war while under enemy occupation. Food and fuel had been abundant but this winter is harsh – harsher than most. As other comforts become scarce, so too does the food supply so the people must rely on rations. But Winter continues and the enemy remains. The food stores plummet further. Where the average adult needs between 2,200 and 2,600 calories, those suffering the famine’s peak receive a meagre daily ration of 400 calories a day. This is the Dutch Hunger Winter. The Netherlands was liberated from enemy occupation just as food stores ran out but though the famine ended, it’s impacts were still felt many years later. When studies were conducted on the children of women who had been pregnant during the famine, scientists found they had a lower tolerance for sugars later in life, making them more susceptible to type 2 diabetes.

Similarly, another study found connections between birth rate and disease in middle-aged men from the UK. Issues with sugar uptake were seen in those men that had low birth weights, with a greater number of them dying from heart disease. This same pattern was observed in populations all over the world. Clearly, stresses felt by the mother and birth weight was having an impact on the likelihood of developing diseases later in life.

The increased risk to issues like heart disease and type 2 diabetes can be linked to changes in the way the body would normally use energy. When a pregnant woman suffers a lack of nutrition, the child obviously feels the effects of this. But the amazing part is the way the child’s body responds while still in the womb: it goes into survival mode.

Cue epigenetics.

The reduced nutrient uptake in the mother is translated as the environment outside the womb being harsh and without a good supply of resources. The fetus’ body responds by makes arrangements so that it might better cope with the looming post-birth hardship. This often means reduced energy use, greater calorie storage and in turn faster development. This particular way of functioning can be called the Thrifty phenotype. Now this would greatly improve a child’s survival if the environment was as harsh as the body assumed. But when the environment is actually rich in resources as it is in most Western societies, all that energy storage becomes a problem. When energy isn’t used it leads to issues like diabetes, heart disease and type 2 diabetes. And so the dietary problems experienced by the mother cause epigenetic changes in the young that make them more vulnerable to diseases during their adult lives.

The conditions a mother is exposed to can have huge affects on her child that are felt well into adulthood. The diet part of epigenetic changes is just the surface of the matter. There is so much more to epigenetics, an aspect of biology acting on us from the very first days of life.