Genetic risk, low diet quality increase type 2 diabetes risk
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Genetic risk and poorer diet quality each independently increase the risk for developing type 2 diabetes, according to study data.
“Our study is the first to investigate how genetic risk and diet quality impact the development of type 2 diabetes,” Jordi Merino, PhD, a research fellow at the Center for Human Genetic Research at Massachusetts General Hospital, told Healio. “We confirmed data from previous small studies showing that both genetics and diet quality are independently associated with the risk of developing the disease.”
For the study, Merino and fellow researchers aimed to elucidate what he called an “intriguing and unanswered question” concerning whether there is a synergic effect between genetic risk and diet.
The study included data from 35,759 U.S. adults who participated in the Nurses’ Health Study I (1986 to 2016) and II (1991 to 2017) and the Health Professionals Follow-up Study (1986 to 2016), totaling 902,386 person-years of follow-up. Participants had available genetic data and did not have diabetes, cardiovascular disease or cancer at baseline.
Researchers characterized genetic risk via both a global polygenic score and pathway-specific polygenic scores and determined diet quality with the Alternate Healthy Eating Index (AHEI).
In all, 4,433 participants were diagnosed with type 2 diabetes. With each standard deviation increase in global polygenic score, the RR for type 2 diabetes was 1.29 (95% CI, 1.25-1.32; P < .001). With each 10-unit decrease in AHEI, the RR for type 2 diabetes was 1.13 (1.09-1.17; P < .001).
Compared with high diet quality, low diet quality yielded an approximately 30% increase in risk for type 2 diabetes (P for interaction = .69) regardless of genetic risk. Researchers also observed that the joint association of low diet quality and increased genetic risk was comparable to the sum of the risk associated with each factor alone (P for interaction = 0.3).
“Altogether, our results are essential to understanding why people develop diabetes and support evidence-based prevention strategies for type 2 diabetes,” Merino said.
He added that the study is novel in that it considered several genetic risk scores to capture overall genetic risk and specific molecular processes leading to diabetes.
“In addition, we used modern epidemiological methods to investigate different types of interactions between diet and genetics,” he said. “Further, our study used multiple measurements of diet during the follow-up (20 years) to reduce measurement error and biases.”
He concluded that from a public health perspective, the findings suggest that “public health policies should be targeted to promote healthy dietary recommendations at the population level. Our results also emphasize the value of genetic risk assessment to identify individuals at increased disease risk and their potential for risk stratification and surveillance.”
For more information:
Jordi Merino, PhD, can be reached at jmerino@mgh.harvard.edu; Twitter: @riudecanyenc.
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