In the past century, Austria experienced three major famines. Now researchers suggest those born in these times of hunger suffered from excess risk for diabetes, according to a paper published in PNAS Early Edition.
In 1918, at the end of World War I, the Austro-Hungarian Empire collapsed spectacularly, and the resulting modern state of Austria lost all food supplies from its former member states and at the same time was under embargo by the Allies. In 1938, hunger struck again due to economic crisis, and in 1946 and 1947, famine occurred in the aftermath of World War II.
Scientists analyzed more than 325,000 Austrian patients under pharmaceutical treatment for diabetes during 2006 and 2007. They found a massive excess risk of diabetes, mainly type 2, in people born during and immediately after the three major famines in 20th-century Austrian history.
“When we first saw the results, I was sure this was an error in the data,” says researcher Stefan Thurner at the Medical University of Vienna. “The exciting thing was the cleaner we got the data, the bigger the effect got.”
For instance, in extremely poor provinces of Austria, there was up to more than twice as great a chance of having diabetes when born in 1919 to 1921, compared with people born in the year before and the year after. In comparison, the excess risk for diabetes was practically absent in richer provinces less hit by hunger.
“This is not only a significant effect, this is huge,” Thurner says.
Past research has suggested that malnourishment in early life can have long-lasting effects on health. For instance, scientists analyzing the effects of the Dutch Hunger Winter, the Great Chinese Famine and the Biafran Famine during the Nigerian Civil War hinted at problems in adulthood such as diabetes. However, these past studies were each limited to only a few thousand subjects each, far less than this new work.
“Our research suggests that when the mother suffers hunger, the baby becomes diabetic in later life,” Thurner says.
A notion known as the thrifty phenotype hypothesis suggests depriving children of sugar early in development may lead developing fetuses to adopt strategies that assume continued poor nutrition after birth. This could then leave them ill-prepared for what are generally considered normal levels of glucose. For instance, they may suffer difficulties linked with the pancreatic beta cells that store and release insulin—about half of all adult beta
cells have already developed by the first year of life.
Males in the study also showed a consistently higher overall risk of diabetes. This might be due to sex-related differences in lifestyle and health—for instance, men are more likely to be overweight and are more insulin-resistant. Thurner and his colleagues note that recent research also hinted males may suffer especially if subjected to malnutrition during pregnancy due to possible sex-linked epigenetic differences.
If hunger-linked diabetes is real, “this would mean that in places where pregnant women suffer hunger today, one should expect significantly higher diabetes rates in the next 30 to 50 years,” Thurner says. Physicians may want to screen for people who were born in times of hunger at an early age and start treatment much earlier than now, he adds.
The scientists now want to systematically analyze data on all treated diseases in Austria to discover unexpected patterns. “These data are basically a way to completely map a national health system,” Thurner says. Such research might also shed light on the epidemics of obesity, diabetes and cardiovascular disease now seen afflicting many developed countries today, he notes.