Dear Dr G,I read with interest your article about the diagnosis of Premature Ejaculation.I am a man in my early fifties and I am rather curious about having such a problem in my old age.My wife and I had a normal sexual relationship since we were married in our mid-twenties.Sadly, she passed away a few years ago and I did not engage in any intimate relationships until I recently met a co-worker.To my surprise, I began to notice I ejaculate a lot faster than how it used to be.Admittedly my partner is a lot younger than me and I am somewhat out of practice.However, I still cannot work out how my sexual timing was normal before.What better way to start the new year than by putting Dr G on the spot for clarification over the timing matters of sex!First of all, can you tell me what causes Premature Ejaculation?Is Premature Ejaculation purely a psychological dysfunction?Can this sexual dysfunction be associated with any illnesses?And lastly, why was I normal and now so fast in bed?Yours truly,Fast Fabien Premature ejaculation is a complex male sexual disorder whose pathogenesis reflects an interplay between biological vulnerability and acquired modifying factors. Contemporary understanding no longer frames it as a purely psychological condition but rather as a disorder of ejaculatory threshold regulation, in which central neurobiological control, peripheral sensory input, autonomic balance, and contextual psychological influences converge. Appreciating this multifactorial pathogenesis is essential, because correct identification of the underlying etiology directly determines effective treatment. At the core of premature ejaculation lies dysregulation of central serotonergic neurotransmission. Serotonin exerts an inhibitory influence on ejaculation through specific receptor subtypes within the brain and spinal cord. Reduced serotonergic tone, increased sensitivity of excitatory serotonin receptors, or diminished activity of inhibitory receptors lowers the ejaculatory threshold, resulting in rapid ejaculation with minimal stimulation. This neurobiological vulnerability explains why many men with lifelong premature ejaculation experience symptoms from their first sexual encounters and why pharmacologic agents that enhance serotonergic signaling reliably prolong ejaculatory latency. Genetic polymorphisms affecting serotonin transporters and receptors further support the concept that, in a substantial proportion of men, premature ejaculation represents a constitutional neurophysiological trait rather than a learned behavior. Peripheral mechanisms may amplify this central vulnerability. Increased penile sensory input, particularly from the glans penis, can accelerate afferent signaling to spinal ejaculatory centers, triggering ejaculation before higher cortical inhibition can intervene. Evidence for this mechanism includes heightened penile sensitivity on sensory testing and partial therapeutic responses to topical anesthetics. In some men, hyperexcitability of the spinal ejaculatory reflex itself appears contributory, leading to reflexive ejaculation that is poorly modulated by voluntary control. Hormonal and systemic factors play a particularly important role in acquired premature ejaculation. Hyperthyroidism, for example, increases adrenergic tone and sensitises the ejaculatory reflex, and normalisation of thyroid function often restores normal ejaculatory latency. Urogenital inflammatory conditions such as chronic prostatitis or urethritis can also shorten ejaculation time through local irritation and heightened reflex sensitivity. Erectile dysfunction frequently coexists with premature ejaculation, not as a primary cause but as a reinforcing factor, where fear of losing erection promotes hurried sexual activity and rapid climax. Psychological factors, while historically overemphasised, are best understood as modulators rather than primary drivers in most cases. Performance anxiety, relationship conflict, early conditioning to rapid ejaculation, and hypervigilant monitoring of sexual performance can all increase sympathetic nervous system activity and further lower ejaculatory control. These factors are particularly prominent in acquired premature ejaculation and may perpetuate symptoms even after an initial biological trigger has resolved. Etiological clarification requires targeted clinical evaluation. Assessment of thyroid function, screening for prostatitis or other urogenital pathology, and evaluation for erectile dysfunction help identify reversible medical contributors. Focused questions regarding penile sensitivity, response to condoms or topical agents, and changes in sexual arousal patterns can suggest a significant peripheral sensory component. Psychological assessment should explore anxiety, depressive symptoms, relational dynamics, and maladaptive sexual beliefs, not as presumptive causes but as factors that may sustain or exacerbate the condition. Premature ejaculation arises from a lowered ejaculatory threshold driven primarily by central serotonergic dysregulation, with genetic predisposition, peripheral hypersensitivity, spinal reflex hyperexcitability, hormonal influences, and psychological modulation contributing to varying degrees. Accurate identification of etiology depends on careful differentiation between lifelong and acquired forms, comprehensive sexual and medical history-taking, and selective investigation of biological and psychosocial factors. This etiological clarity is essential, as it transforms premature ejaculation from a vague complaint into a treatable condition with rational, targeted therapeutic strategies. Comedian Groucho Marx, one of the famous Marx Brothers, once said: “Early to bed and early to rise makes a man healthy, wealthy but grumpy.” Men who face late onset of early ejaculation often put Dr G on the spot for some explanation. His view is: “Despite being healthy and having a wealth of experience, unexplained early climax can still make men very grumpy!”
