The practice of edging involves maintaining a high state of sexual arousal for an extended duration while deliberately avoiding the point of climax. This technique aims to prolong pleasure or delay ejaculation. Testosterone, the primary male androgen, is a steroid hormone produced mainly in the testes that regulates libido, muscle development, and overall energy. Widespread speculation and myths exist concerning edging’s ability to significantly alter the body’s testosterone levels. This exploration aims to clarify the physiological reality of how this sexual practice interacts with the endocrine system.
Understanding Testosterone and Sexual Arousal
Testosterone production is tightly controlled by the Hypothalamic-Pituitary-Gonadal (HPG) axis, a complex feedback loop connecting the brain and the testes. The hypothalamus releases gonadotropin-releasing hormone, which prompts the pituitary gland to secrete Luteinizing Hormone (LH). LH then travels through the bloodstream to the testes, stimulating the Leydig cells to synthesize and release testosterone. This hormone plays a foundational role in general health maintenance, affecting bone density, fat distribution, and red blood cell production, in addition to its influence on sex drive.
During typical sexual activity leading to ejaculation, testosterone levels experience a transient but noticeable increase. Serum testosterone can rise significantly from the moment of erection up to the point of climax. This temporary spike reflects the heightened physiological state of arousal and anticipation. However, this elevation is short-lived, with levels often returning to the pre-arousal baseline within minutes after ejaculation.
The Acute Hormonal Response to Edging
Edging extends the plateau phase of the sexual response cycle, maintaining the body in a sustained state of intense, pre-ejaculatory arousal. Since standard sexual arousal causes a temporary rise in testosterone, the prolonged high-arousal state associated with edging effectively extends this period of elevated hormonal activity. This sustained elevation is driven by the continued stimulation of the HPG axis, which continues to signal for testosterone production to support the prolonged sexual engagement.
However, the notion that edging causes a sustained surge in testosterone is a misconception. The resulting increase in circulating testosterone is considered minor and acute, representing a temporary deviation from the individual’s normal daily range. Compared to the systemic factors that genuinely influence hormone health, such as consistent sleep, regular resistance exercise, and proper nutrition, the hormonal effect of edging is relatively insignificant. Research on sexual abstinence suggests that while testosterone levels may be slightly higher after a period of abstinence, the difference is generally not large enough to translate into meaningful physiological changes for performance or muscle building.
Prolactin and the Post-Climax Hormonal Shift
The perceived difference in energy and libido after edging is often less about a testosterone increase and more about the avoidance of a post-ejaculatory hormonal cascade. Ejaculation typically triggers a significant release of the hormone prolactin from the pituitary gland. This prolactin surge is strongly associated with the post-coital refractory period, which is the time required before a male can become aroused again.
By avoiding ejaculation, the practice of edging bypasses this substantial prolactin spike. The absence of this hormone surge helps prevent the immediate onset of the refractory period and the accompanying loss of sexual desire. Other neurohormones like oxytocin and vasopressin are also released during climax, contributing to feelings of bonding and post-coital relaxation. Edging prevents or modifies the full release of these hormones, which contributes to the subjective experience of feeling more energized and quickly able to return to a state of arousal, an effect often mistakenly attributed to high testosterone levels.