Words: Nina Atkinson (she/her)
The unborn, it seemed, were not insulated from the effects of history.
In a Glasgow GP surgery, a second-generation South Asian student is informed that she faces an elevated statistical risk of cardiovascular disease. “Ethnicity” is listed among the risk factors. We tend to treat risk as contemporary. Shaped by factors like diet, movement, or personal choice. The leaflet offers no reference to famine or displacement; the explanation appears immediate. The body, however, may have a longer memory.
The legacies of the Empire are usually discussed in political and economic terms. Modern patterns of global inequality, uneven development, and instability are frequently traced back to colonial rule. But not all legacies announce themselves so clearly. Some are folded into ordinary clinical language. South Asians in the UK are statistically more likely to develop Type 2 diabetes, often earlier than their white European counterparts. Increasingly, research suggests that this pattern may partly reflect metabolic adaptations formed in times of extreme deprivation and passed quietly across generations.
In the late 20th century, epidemiologist David Barker proposed what became known as the “Developmental Origins of Health and Disease” hypothesis. This theory suggested that conditions experienced in the womb influence long-term susceptibility to illnesses such as heart disease and diabetes. Poor prenatal nutrition does not simply produce smaller babies, but can impact disease-risk factors. Striking evidence came from the Dutch Hunger Winter of 1944-45. When Nazi blockades cut off food supplies to the western Netherlands, rations dropped as low as 400-800 calories. Around 20,000 people died, and millions endured severe starvation. The meticulous keeping of medical records from this incident has allowed researchers to later study its long-term effects.
Individuals exposed to famine in utero were more likely to develop Type 2 diabetes, cardiovascular disease, and certain mental health disorders as adults. Some effects appeared to extend to their children. The population had been well-nourished both before and after the famine, pointing to gestational hunger as the critical variable. The unborn, it seemed, were not insulated from the effects of history.
The mechanism is often cited as “epigenetics.” In epigenetics the DNA sequence does not change in response to famine, but instead ‘tags’ onto the genes, influencing whether they are switched on or off. In conditions of scarcity, promoting energy conservation and fat storage are adaptive responses, but in modern calorie-abundant environments, they can cause an increased risk of obesity and diabetes.
Starvation under colonial rule was not simply a natural disaster, but was shaped by governance. Food remained available in British India during the period of the 1943 Bengal Famine, but wartime priorities, grain exports, and failures of distribution meant that food did not reach those who needed it most. An estimated 3 million people died.
The legacies of famine are not just felt by those who directly experienced it. Emerging research has suggested that epigenetic shifts may have altered metabolic risks across generations. Studies of certain populations exposed to severe hunger – including South Asians and their diaspora – have shown increased susceptibility to hyperglycaemia and cardiometabolic disease in adulthood.
A similar pattern can be seen in descendants of the Great Famine in Ireland, which killed one in eight, and forced the mass emigration of many others. The Irish case is harder to track due to this mass displacement, but there is evidence for some link to later cardiovascular and metabolic vulnerability. Similarly, Indigenous populations in North America have elevated risks of diabetes, heart disease, and psychiatric distress. This is often thought to be linked to the forced displacement, food system disruption, and chronic stress faced by their ancestors under colonisation. In these instances, the details may differ, but the through-line remains consistent. There are long-term biological consequences to systemic enforced deprivation.
Famine is not just a historical phenomenon. In several parts of the world today, access to food is constrained not by absolute scarcity but by conflict or political decision-making. Given what we know about the effects of prenatal malnutrition, it leads us to question how future generations will be impacted in places still facing state-sanctioned famine even now, such as the people of Gaza. Crises do not end when ceasefires are signed or headline attention fades, their effects persist at a cellular level for generations to come.
Souvenirs are often thought of as cherished objects we bring back from places we have left. But metabolic adaptations do not sit on shelves as reminders of finished journeys. Instead, they live quietly within bodies altering the health of populations for generations. Empires may fall. People may momentarily forget the pain inflicted upon their ancestors. Yet the body, adapting to survive, keeps a quiet record. The past, it turns out, is not just the past, but is presently circulating through our veins.
