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China famine babies: Hyperglycaemia and diabetes risk passes down to second generation too

By Gary Scattergood+

13-Dec-2016
Last updated on 13-Dec-2016 at 04:05 GMT2016-12-13T04:05:24Z

Experts believe up to 45m people died due to the famine between 1959-61.
Experts believe up to 45m people died due to the famine between 1959-61.

An increased risk of high blood glucose levels and diabetes is not only greater for people who were born at a time of famine, but it is also then passed down to their children, research into China’s 1959-1961 food crisis has discovered.

The new study in the American Journal of Clinical Nutrition reports that hundreds of people who were gestated during the famine that afflicted China between 1959 and 1961 had significantly elevated odds of both hyperglycaemia and type 2 diabetes.

The study also found that their children also had significantly higher odds of hyperglycaemia, even though the famine had long since passed when they were born.

Researchers at Brown University and Harbin Medical University in China were able to make the findings by studying more than 3,000 local residents and their children.

The study states: “A total of 1034 families, including 2068 parents [parental generation (F1)] and 1183 offspring [offspring generation (F2)], were recruited from the Suihua rural area that was affected by the Chinese Famine of 1959–1961. Participants born between 1 October 1959 and 30 September 1961 were defined as famine exposed, and those born between 1 October 1962 and 30 September 1964 were defined as nonexposed.

“The F2 were classified as having 1) no parent exposed to famine, 2) only a mother exposed to famine, 3) only a father exposed to famine, or 4) both parents exposed to famine. Classical risk factors for T2D as well as fasting-glucose- and oral-glucose-tolerance tests were measured in both the F1 and F2.”

Among 983 people gestated during the famine years, 31.2% had hyperglycaemia and 11.2% had type 2 diabetes.

By comparison, among 1,085 people gestated just after the famine ended, the prevalence of hyperglycaemia was 16.9%, and the prevalence of type 2 diabetes as 5.6%.

Controlling for factors such as gender, smoking, physical activity, calorie consumption and body-mass index, the researchers calculated that in utero famine exposure was associated with 1.93-times higher odds of hyperglycaemia and a 1.75 times greater chance of type 2 diabetes.

The next generation sustained the significant risk of hyperglycemia when both parents had been famine-exposed. Overall in the second generation, hyperglycaemia prevalence were 5.7% for 332 people with no famine-exposed parents, 10.0 percent for 251 people with famine-exposed fathers, 10.6% for 263 people with famine-exposed mothers, and 11.3% for the 337 people for whom both parents had famine exposure.

Substantially elevated

Adjusting for all the same lifestyle factors, the offspring of two famine-exposed parents had 2.02 times the odds of hyperglycemia of people with no famine-exposed parents. The odds of hyperglycaemia from one-parent exposure were also substantially elevated but not quite statistically significant.

The odds of type 2 diabetes were not statistically significant after adjustment for multiple comparisons among the second generation, but co-corresponding author Dr. Sun Changhao, professor of nutrition and dean of the School of Public Health at Harbin, noted that these people were only in their 20s and 30s and could still be at increased risk as they age and that the research team will continue to follow up on these participants.

Because the study only shows an association between metabolic changes and in utero famine exposure, it can't prove causality or the biological mechanism underlying a cause. But prior research on the effects of famine in humans and in laboratory animals suggest that famine does indeed cause such health risks, the study authors said.

"It is indeed a remarkable finding that is consistent what with what one would have expected from prior findings from animal experiments," said lead author Jie Li, a Brown postdoctoral fellow.

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