|The Chinese Famine (1959-1961) left health effects on|
people who were in utero at the time. Image: China Mike
The review, led by Department of Diabetes Professor Paul Zimmet AO, examined data about in utero exposure to poor nutrition during the Chinese Famine (1959–1961), concluding it probably contributed to China's current diabetes epidemic.The paper warns that relief agencies should urgently review the way emergency food aid is given in populations during major catastrophes, including war and earthquakes.
by Professor Paul Zimmet AO
Time in the womb is a critical period for early childhood development. Major famines and other disasters can determine the future risk of the baby in the womb of developing diabetes, obesity and heart disease as adults. The impact on the baby’s pre-birth nutrition resulting from famine induced malnutrition in the mother is an important trigger.
Catastrophic famines may be important drivers of the global type 2 diabetes epidemic. Diabetes is arguably the largest chronic disease epidemic in modern history. Recent global diabetes numbers, certainly underestimates, suggest there were 449 million people with diabetes in 2017 rising to over 700 million by 2045.
China provides a powerful example of this scenario as prenatal exposure to the Chinese Famine (1959-1961) has been associated with increased risk of diabetes in adulthood in two successive generations. Over 25% of all cases of diabetes globally are now in China. Forty years ago, diabetes was uncommon then yet today there are over 120 million people affected. China has over 25% of all diabetes globally.
What has driven this dramatic increase? Genes and lifestyle change, the traditional “culprits”, do not explain this phenomenal increase. How harmful early life events invoke increased diabetes risk is explained by epigenetic changes. Epigenetic change may occur during lifetime being influenced by age and environmental factors including dietary exposures. These changes in gene expression do not involve structural change of the gene but a biochemical modification. This is different to the accepted Mendelian proposal of genetics. Epigenetic changes can become intergenerational, conveying risk of diabetes and obesity in adulthood, thus perpetuating risk through future generations.
The association between famine and type 2 diabetes is not limited to China. Rises in diabetes numbers occurred many years after famines in the Netherlands (The Dutch Winter Famine), the Ukraine and elsewhere.
The famine and diabetes scenario, a rise in diabetes seen many decades after catastrophic famines, provides an urgent public health warning. It has important implications for diabetes control in the developing world. In China alone, the current epidemic now poses huge social, health and economic challenges that could threaten national development through disability and premature morbidity from diabetes.
This warrants a very strong and urgent call for UN Food Agencies and other to review the way emergency food and nutritional aid is handled in populations for major catastrophes. This applies not just for famines and earthquakes but also where political and ethnic conflicts exist such as the Horn of Africa and Syria.
The future welfare and lifecourse of millions of children depend on action on the urgent need for responsible and appropriate handling of the nutritional and social issues in terms of relief aid and food supplies. The lessons from the Dutch, Chinese and other famines need to be heeded.
Billions of dollars have been spent with limited success searching for key genes causing type 2 diabetes, a task likened to searching for a needle in a haystack. Therefore, research to develop drugs to neutralise epigenetic changes is now a high priority for health and humanitarian reasons.
The paper entitled Epidemic T2DM, early development and epigenetics: implications of the Chinese Famine was co-written by Associate Professor Zumin Shi, who contributed equally with Professor Zimmet and who works in the Human Nutrition Department, Qatar University; Professor Assam El-Osta, Monash Department of Diabetes; and Professor Linong Ji, Peking University Diabetes Council, Peking University, Beijing, China.