Genetic risk factor for erectile dysfunction identified
In a first, researchers have found a specific place in the human genome that raises a persons risk of erectile dysfunctionResearchers from the USbased Kaiser Permanente have found variations in genetic locus near the SIM1 gene were associated with 26 per cent increased risk of erectile dysfunction
New York: In a first, researchers have found a specific place in the human genome that raises a person's risk of erectile dysfunction.
Researchers from the US-based Kaiser Permanente have found variations in genetic locus -- near the SIM1 gene -- were associated with 26 per cent increased risk of erectile dysfunction.
"Identifying this SIM1 locus as a risk factor for erectile dysfunction is a big deal because it provides the long sought-after proof that there is a genetic component to the disease," said Eric Jorgenson, research scientist at the varsity.
"Identifying the first genetic risk factor for erectile dysfunction is an exciting discovery because it opens the door for investigations into new, genetic-based therapies."
For the study, published in the journal Proceedings of the National Academy of Sciences, the team included 222,358 men.
The findings revealed that the SIM1 locus was indeed a risk factor for erectile dysfunction, whether the disorder was defined through clinical diagnoses, prescriptions history, or study participant self-report.
The study highlights the potential of SIM1 as a target for the development of new treatments for erectile dysfunction, which are needed because about half of all men who try currently available pharmaceutical treatments for erectile dysfunction do not respond to them.
Therapies based on these factors exist, but many men do not respond to them, the researchers said.
Genetics are also suspected as a factor in about one-third of erectile dysfunction cases, but researchers have failed to make an association with any specific genomic locations until now.
"This study points to a new research direction for erectile dysfunction that could help us identify other key genetic variants that trigger the disease and lead to investigations to better understand the precise mechanisms by which they operate," explained Hunter Wessells, at the University of Washington.