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Response to Commentary on Rowland et al. “Similarities and differences between men with self-reported lifelong and acquired difficulty reaching orgasm”

International Journal of Impotence Research (2023)Cite this article

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A Comment to this article was published on 10 October 2023

The Original Article was published on 10 October 2023

We appreciate that Perelman has read our paper “Similarities and Differences between Men with Self-Reported Lifelong and Acquired Difficulty Reaching Orgasm” [1] and taken the time to offer his clinical perspective on the issue in his commentary [2]. For the most part, we concur with his comments and, in some instances have already addressed the issues that he raises in other published studies. But we also note Perelman has commented not only on the study that we carried out, but also on a study that he hopes we carry out in the future. Thus, we begin by reiterating that the scope of our paper was limited to identifying similarities and differences between men with self-reported lifelong vs acquired delayed ejaculation (DE). As such, this study represents the most comprehensive analysis of such differences to date, using a robust sample of men indicating difficulty reaching orgasm (or DE): it included assessments of sexual, relationship, and behavioral variables, as well as variables related to reasons for masturbation, ascribed/attributed reasons for difficulty reaching ejaculation, and the types of activities engaged in during partnered sex and (separately) masturbation. We were not comparing men with difficulty reaching orgasm to men without such difficulties, and we have not suggested that men with different DE subtypes might not also differ on variables beyond the scope of our analyses; however, we believe we have captured some of the most relevant variables.

Having made the above point, we turn to the specific issues raised by Perelman. First, the idea that ejaculation latency (EL) for men with DE might be biologically or genetically predisposed is an assumption that has been made by many who study this topic, including ourselves. However, it is just that—an assumption. We do not dismiss the “predisposition” idea in our paper, but merely note that the assumption currently lacks empirical evidence; that is, to our knowledge, no convincing data have ever been presented that unequivocally demonstrate hard-wiring differences in the ejaculatory pathways of men with ejaculatory disorders (e.g., premature ejaculation (PE) and DE) compared with men without ejaculatory disorders. Indeed, the one study investigating a biological/genetic predisposition for DE generally failed to provide supporting evidence [3]. On the other hand, we do not assume that because there is a lack of current evidence for such a disposition that one may not exist—we simply note that in the absence of evidence, lifelong DE, as with lifelong PE, may be best viewed as idiopathic. Perelman, in his commentary, offers a model and arguments based on assumptions of how physiological (endocrine, neural) systems might or could be involved in mediating ejaculation latency, and we agree with such possibilities.Footnote 1 But without supporting evidence, statements regarding biological predispositions, while offering convenient (and sometimes clinically useful) ways of explaining variation in ejaculation latencies to patients, devolve into an exercise on circular reasoning—as researchers, we note variation in EL and attempt to identify its causes, including “presumed” ones that might be biological. But then we use these same presumed biological causes to explain the variation in ELs—such circularity does not advance scientific thinking. In the absence of any clearly identified causes for lifelong DE, one could just as readily argue that variation in ejaculatory latencies is based on “soft-wired” transient neural processes such as levels of psychosexual arousal [4, 5]. Indeed, given that therapists are in a position to manipulate only non-biological factors related to ELs, we and Perelman undoubtedly agree that psychological factors may not only be key to understanding some aspects of sexual functioning and dysfunction, but that in some instances they offer the best opportunities for change or modification of a response, for example, when physiologically-altering medications are unavailable.

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Notes

  1. The field of behavioral genetics often uses a mix of biological dispositions and experiential/environmental factors to explain outcomes, with genetics (via biological structure) setting the lower and upper limits, and experience establishing the set point within those limits. While such a model is appealing as a way of explaining ejaculatory disorders, the essence of the behavioral genetic interpretation necessitates the identification of specific genetic or genetically-related factors to support such an interpretation. Such evidence is currently lacking for DE.

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Authors and Affiliations

  1. Department of Psychology, Valparaiso University, Valparaiso, IN, USA

    David L. Rowland

  2. Department of Applied Health Science, School of Public Health, Indiana University, Bloomington, IN, USA

    Sean M. McNabney

  3. Institute of Psychology, Eötvös Loránd University, Budapest, Hungary

    Krisztina Hevesi

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  2. Sean M. McNabney
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  3. Krisztina Hevesi
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Correspondence to David L. Rowland.

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Rowland, D.L., McNabney, S.M. & Hevesi, K. Response to Commentary on Rowland et al. “Similarities and differences between men with self-reported lifelong and acquired difficulty reaching orgasm”. Int J Impot Res (2023). https://doi.org/10.1038/s41443-023-00770-w

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