Genetic Cause Linking Erectile Dysfunction and Type 2 Diabetes Discovered

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For men who suffer from erectile dysfunction, it can cause extraordinary emotional distress, disrupt relationships, and be a red light for other serious health conditions such as circulation and blood pressure problems.

Our new study, published in the American Journal of Human Genetics, shows that erectile dysfunction (ED) has a genetic component. We found strong evidence of a link between certain parts of DNA and the ability to develop and maintain an erection; ED is estimated to affect 20-40% of men between the ages of 60 and 69, and this ability naturally declines with age.

We also found that an increased risk of type 2 diabetes (based on many different genes) also causes ED.

Our study utilized data from the UK Biobank of men of European ancestry and, to draw conclusions from a broader sample, compared and combined them with data from the Estonian Genome Center at the University of Tartu and men drawn from the Partners Health Care Biobank in the United States The data were compared and combined.

The UK Biobank is a remarkable storehouse of genetic and medical data available to scientists. Funded by philanthropic organizations and government agencies, 500,000 people between the ages of 40 and 69 were recruited from across the country between 2006 and 2010. These volunteers completed many detailed questionnaires, provided measurements, blood, urine, and saliva samples, and kept follow-up appointments over the years.

Many have also been fitted with activity monitors and undergone medical scans. They also agreed to allow researchers to access their hospital records and prescription information. The result is a very rich trove of data that can be used to answer many questions related to health, well-being, and risk of future health conditions.

Digging into the Data
Because of the sensitive nature of this particular medical problem, it is perhaps not surprising that few people self-report experiencing ED. To maximize the chances of finding a genetic cause, we combined self-reported individuals with those taking ED medications such as Viagra and those who had undergone surgery to address ED-related health issues. Using this approach, we identified 6,175 ED men in the UK Biobank.

The DNA of these participants was then compared to the remaining 223,805 men in the Biobank who were not classified as EDs to see what differences and similarities could be detected. They found very strong evidence that genetic location was responsible for the slightly increased risk of EDs. Interestingly, we also found evidence that as the risk of type 2 diabetes increases, the risk of ED also increases.

Indeed, type 2 diabetes has long been associated with ED, but not at the genetic level. It has generally been thought that this may be due to obesity and other metabolic problems that type 2 diabetes tends to cause, its effect on the blood vessels of the penis, and thus on the maintenance of erections. What our study has shown is that people who are genetically at higher risk for type 2 diabetes are also at higher risk for ED, suggesting that T2D is a likely cause of ED. This suggests that T2D is a likely cause of ED.

Which gene increases the risk of ED?

The gene we believe increases the risk of ED is called Sim1. Specifically, changes in the way this gene works increase the risk of developing ED. Previously, changes in this gene have been associated with nervous system problems that affect severe obesity and blood pressure. We observed this condition in our participants, providing further evidence that this gene is involved in ED.

There is some evidence from mouse studies that brain cells lacking Sim1 are responsible for reduced sexual performance. In short, our study suggests that the genetic risk we have identified may cause ED not due to obesity, but by affecting the brain and nervous system, particularly the hypothalamus, which controls many unconscious bodily functions, including breathing, heart rate, and sexual response.

Why is this a problem if we can’t change our genes?Understanding the causes and risk of developing conditions such as ED may help us to better advise and treat our patients. This new genetic knowledge may provide opportunities to develop new drugs to treat EDs, to examine how existing drugs can be used earlier in patients, and to predict a man’s likelihood of developing EDs. The independent effects of BMI and ED also suggest that men are at risk for ED regardless of their weight.

Unfortunately, as with the majority of genetic studies, these findings most certainly apply to patients of European descent. The frequency of the genetic alterations we found is approximately 23% in individuals of European descent, compared to 0.1% to 34% in other ethnic groups. Given this disparity, a biobank with data from volunteers from a wider range of ethnic backgrounds is needed to get a complete picture.

Fortunately, our results have also been observed by a research group in the United States. Using data from the Kaiser Permanente Northern California Biobank, which includes a small but multi-ethnic population, the group recently demonstrated that Sim1 is involved in EDs.

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