Premature and Delayed Ejaculation: Genetic and Environmental Effects in a Population-Based Sample of Finnish Twins

Abstract

Introduction A number of different theoretical approaches to understanding the etiology of ejaculatory dysfunction have been proposed, but no behavior genetic study has yet, to our knowledge, been conducted to explore the genetic and environmental influences on ejaculatory dysfunction. Aim The aim of the present study was to explore the genetic and environmental effects on premature (PE) and delayed (DE) ejaculation in a population-based sample. Methods The genetic and environmental influences on PE and DE were investigated in a population-based sample of 1,196 Finnish male twins, age 33–43 years, with 91 identical and 110 complete twin pairs. Several different aspects of ejaculatory function were measured by a self-report questionnaire (e.g., latency time, subjective experience of ejaculatory control). Factor analyses distinguished two subcomponents of ejaculatory function, and subsequently, composite variables measuring PE and DE were created. Structural equation modeling was performed on the composite variables. Main Outcome Measures Measurement of genetic and environmental effects on PE and DE. Results The results suggested moderate genetic influence (28%) on PE, but not on DE (0%). There was a moderate familial effect on DE with shared environmental effects accounting for 24% of the variance. However, omission of the shared environmental component did not directly result in a significantly decreased model fit for DE, and omission of the additive genetic component did not directly result in a significantly decreased fit for the PE model. Conclusions The findings from the present study provide useful information regarding the etiology and understanding of ejaculatory dysfunction.

Evidence for a genetic etiology to ejaculatory dysfunction

“…In continuation of the results of Jern et al, 10 PE was expected to be under moderate genetic influence, whereas no such effects were expected for DE. Instead, shared environmental factors were hypothesized to have some effect on DE.…”

“…To avoid heterosexist bias and exclusion of both female-male and malemale anal intercourse, we used a gender-neutral definition of ejaculation latency time inclusive of anal intercourse. The questions were adapted from an unpublished questionnaire developed by Grenier and Byers 19 (see Jern et al 10 for details).…”

“…Therefore, shared environmental factors could also explain a familial occurrence of PE. Jern et al, 10 in a population-based study of Finnish men, found a highly significant familial effect in PE, which strong implications that this effect be genetic. However, they were not able to separate clearly the genetic effects from shared environmental effects, probably because of insufficient statistical power.…”

“…Rosen 12 suggested that DE may be associated with a variety of surgical or medical conditions, and in most cases, the use of antiadrenergic or neuroleptic drugs. Jern et al 10 found a moderate familial effect active in DE, but results were inconclusive regarding separation between shared environmental and genetic effects. Indeed, they concluded that the probability of a genetic etiology in DE is negligible.…”

“…For its etiology, psychological, environmental and contextual factors are all still being considered, 4,5 whereas recent research has focused on neurobiological, 6 endocrine 7,8 and genetic explanatory frameworks. 9,10 In recent years, researchers have tended to favor theoretical approaches that incorporate several different etiological factors to PE. For instance, Waldinger and Schweitzer 11 have proposed a system dividing PE into four subtypes as a function of the intravaginal ejaculation latency time (IELT) and their courses in life.…”