A massive study has found that there is a genetic connection between the two diseases that are the leading cause of global morbidity and mortality – Type 2 diabetes (T2D) and coronary heart disease (CHD).
We’ve known for some time now that T2D is a significant risk factor for coronary heart disease, but the reasons behind this have been somewhat unclear.
Now a huge study by the Perelman School of Medicine at the University of Pennsylvania has revealed the specific changes in our genes that are directly linked to both a higher chance of getting Type 2 diabetes and suffering from coronary heart disease.
The study looked at the genetic sequences of some 250,000 different people.
Within those sequences they discovered 16 new diabetes risk factors and one new CHD risk factor.
They were then able to show that most of the sites on the human genome that are associated with T2D are also associated with a higher risk of CHD, further cementing this link.
For eight of these sites the team discovered a specific gene variant that was tied to both, revealing a key partnership between the two conditions.
Discovering this link is important because it could open up the door to new multi-purpose drugs that tackle both conditions.
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“Identifying these gene variants linked to both type 2 diabetes and CHD risk in principle opens up opportunities to lower the risk of both outcomes with a single drug,” said study co-senior author Danish Saleheen, PhD, an assistant professor of Biostatistics and Epidemiology.
“From a drug development perspective, it would make sense to focus on those pathways that are most strongly linked to both diseases,” Saleheen said.
Interestingly what the team found was that this link didn’t go both ways.
Instead they found that the risk genes for type 2 diabetes were much more likely to be associated with a higher risk of coronary heart disease, rather than the other way around.
So what does this mean for us? Well in the long run, by better understanding these ‘dual-risk genes’ we can create better drugs that can effectively kill two birds with one stone.
“Using evidence from human genetics, it should be possible to design drugs for type-2 diabetes that have either beneficial or neutral effects on CHD risk.” said Saleheen.
Co-senior author Benjamin F. Voight, PhD, believes the next step is to start discovering more of these dual-risk genes and creating a solid understanding of how they work.
“I’m hopeful that with the advanced genomic engineering techniques now available, we’ll be able to quickly convert our human genetics observations into concrete details regarding the molecular mechanisms involved in both heart disease and diabetes,” said Voight.
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