The Kaiser Permanente Health Center in California conducted a study that shows some erectile dysfunction (ED) cases go beyond physical health and the common risk factors: smoking, drinking, and obesity. For some men, the problem is in their genes. (Related topics: urologist in Manhattan)
While short-term fixes for persistent ED like drugs or metal penis implants remain prevalent amongst the wider population, this recent study, published in the Proceedings of the National Academy of Sciences, proposes to focus on identifying the cause of erectile dysfunction, apparently present in a single area on chromosome 6 that seems to control whether a man has to struggle to get an erection or not. Nevertheless, this only works if any other risk factors such as high body weight or alcohol and cigarette use have been ruled out.
In order to carry out this research, the team had to pull out data from 36,649 men at the NIH-funded Genetic Epidemiology Research in Adult Health and Aging cohort and over 222,000 men from the UK Biobank. The data gathered for the study suggests that some men have a slightly different enhancer region known as the T-risk allele and they have a tendency to struggle with sexual function more than men without this distinction. This fact was demonstrated when the teams compared the participants’ genetic information with the data on ED incidence and proved the enhancer’s role in erectile dysfunction in lab experiments. Men who reported a higher incidence of sexual function problems had the higher odds of having this allele.
During the data analysis, the men were split into groups separated as such: the ones reporting “always” being able to get an erection, the ones that claimed “never” managing to do so and two more groups in between. The odds of having ED were 1.41 higher for the men with this gene and the pattern held when they adjusted for other risk factors, like obesity.
A follow-up analysis of the concise function of the enhancer on SIM1, shown by previous studies, shows that regulating hormones is crucial to sexual function. Activation of the enhancer caused cells to express SIM1, whereas controls didn’t — which is important because it suggests scientists can start looking for cells carrying the faulty enhancer allele and narrow in on them as targets for ED treatment.
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