Premature ejaculation and genes

“Premature ejaculation could be passed to men genetically,” the Daily Mail reported. It said researchers have found that men with the condition are more likely to have a genetic abnormality.

The well-conducted research behind this story is based on the plausible theory that a chemical in the brain called dopamine is involved in controlling ejaculation, and that some men may be genetically predisposed to having differences in their levels of this chemical. However, this is unlikely to be the only explanation for the condition, which is a complex problem affected by both psychological and physiological factors. The idea that this variation is a “genetic abnormality”, as claimed by the Daily Mail , is incorrect. It would be more accurate and helpful to view it as a common variation in a well-known gene.

This is early research and the strength of the association between genes and premature ejaculation needs more study. It is not clear how the new knowledge about a genetic involvement in premature ejaculation might help the development of new drug treatments.

Where did the story come from?

This research was carried out by Dr Pekka Santtila and colleagues from university departments in Turku in Finland and Gothenburg and Stockholm in Sweden. The study was supported by grants from the Academy of Finland and from the Stiftelsen för Åbo Akademi Foundation. The study was published in the peer-reviewed Journal of Sexual Medicine.

What kind of research was this?

The study looked at the association between one gene, called DAT1, and premature ejaculation. It was a cross sectional study with a retrospective assessment of premature ejaculation. This means that the men were asked about their history of premature ejaculation at the same time as gene testing was organised, rather than being recruited and tested for the gene and then followed to see how their condition developed (which would be prospective).

The study builds on previous research, which found that ejaculation in humans and animals is in part controlled by levels of the neurotransmitter dopamine in the brain. The researchers say evidence that premature ejaculation has a hereditary component has already been established in twin studies, which found genetic effects accounted for around 30% of the variance in premature ejaculation. This means that, in twin studies, a small but significant part of the condition in a population can be explained by genetics.

This well-conducted research is based on a plausible theory, that dopamine is involved in controlling ejaculation. As this was a small retrospective study, the findings will need to be tested in larger populations that prospectively assess premature ejaculation. Future studies could also investigate whether other genes play a role.

What did the research involve?

The researchers obtained their data from a previous study called the Genetics of Sex and Aggression study. That study was carried out in 2006 and targeted all 18- to 33-year-old twins and their adult siblings living in Finland at the time. Questionnaires were sent to a total of 7,904 male twin individuals and 4,010 of their (singleton) brothers. Of these, 3,923 men (33%) responded. Participants were also asked to provide a saliva sample for DNA analysis, and 1,804 men agreed to do so.

As this present study was not assessing similarities or differences between twins, the researchers randomly excluded one twin from every twin pair and also some men who had incomplete data. This left 1,290 men, 867 of whom were twin individuals and 423 singleton brothers for the final analysis.

The questionnaire asked men to answer four questions related to premature ejaculation. These were adapted from a previously validated questionnaire for this study and included the questions:

In what percentage of sexual intercourse experiences do you involuntarily ejaculate before intercourse has started?
How many thrusts have you typically been able to perform before ejaculation?
On average, during intercourse, how much time elapses between when you first enter your partner with your penis and when you first ejaculate?
How often have you felt that you could decide when to ejaculate?

Background data such as age, frequency of sexual intercourse and homosexuality were also collected.

Responses were scored from one to five. Based on the distribution of responses to these questions, the researchers also developed a composite score, which they used to categorise men as either having premature ejaculation or not.

Participants were also asked to provide a saliva sample for DNA analysis, which was used to analyse which version of the DAT1 gene they carried. The researchers were particularly interested in whether premature ejaculation was associated with different forms (alleles) of the DAT1 gene, called 8R, 9R, 10R, and 11R, which have differing sequences at the end of the gene. Everyone carries two copies of the DAT1 gene, and their “genotypes” describe the combination of alleles they carry. For example, a person with a 9R10R genotype carries one copy of the 9R allele and one copy of the 10R allele.

What were the basic results?

The researchers report that:

36 individuals (2.9%) had the 9R9R DAT1 genotype
396 individuals (31.7%) had the 9R10R DAT1 genotype
816 individuals (65.3%) had the 10R10R DAT1 genotype
The 8R10R and 9R11R genotypes were found in only one individual each, so were excluded from further analysis because of their rarity.

The researchers pooled people with the 9R9R and 9R10R genotypes in their analysis, and compared them with people with the 10R10R genotype. Carriers of the 10R10R genotype had lower scores on three of the four individual questions, meaning that they were more likely to have premature ejaculation than the combined 9R9R/9R10R group.

There was also a significant association between the 10R10R genotype and the men’s composite score. This effect remained significant after taking into account age, homosexual experience, having a regular sexual partner, level of sexual desire and frequency of sexual activity. This means that the effect is likely to be due to a specific influence of the gene on ejaculation rather than some other aspect of sexual behaviour. There was little association between the answers to the individual questionnaire questions themselves.

How did the researchers interpret the results?

The researchers say that their findings support the results of previous studies which indicate the involvement of dopamine in ejaculation.

Conclusion

This study adds further weight to the theory that dopamine plays a role in ejaculation. However, premature ejaculation is due to a complex combination of psychology and physiology, and it is unclear how differences in the DAT1 gene affect it. The researchers note several features that suggest a simple explanation may not be possible:

The strength of the association between the individual questionnaire scores for premature ejaculation was low. As these questions all assessed aspects of premature ejaculation, the scores would be expected to be statistically associated with each other. The fact that they were not casts doubt on this scoring scheme.
The complexity of the underlying mechanisms involved in premature ejaculation is demonstrated by conflicting results of trials into current drug treatment. The researchers give the example of drugs called selective serotonin reuptake inhibitors (SSRIs). These are sometimes used to treat premature ejaculation because of their ejaculation-delaying effect. Users of these drugs apparently, and often surprisingly, report significantly lowered levels of sexual satisfaction alongside increased ejaculation time. The researchers suggest that these contradictory results might be because SSRIs indirectly affect dopamine transmission and delay ejaculation by acting on other neurotransmitters that also reduce sexual satisfaction in some way. The researchers imply that this confirms the condition’s complexity and also means that drugs that directly affect dopamine transmission alone are needed.

The reason that some men experience premature ejaculation could be partially explained by genetic difference. However, it is unlikely to be the only explanation. Calling this variation a “genetic abnormality”, as the Daily Mail did, is incorrect, and it would be more accurate and helpful to view it as a common variation in a well-known gene.