Physicians also use these medications off-label to temporarily pause puberty in adolescents with gender dysphoria (Hughes et al. 2025). GnRH medications are only effective during active treatment and the hormone suppression is reversible (Krebs et al. 2022, Patel et al. 2025). Hormone-pausing medications, or gonadotropin-releasing hormone (GnRH) agonists, are made to look and act like the hormone GnRH (Lahlou et al. 2000). GnRH agonists treat hormone-sensitive cancers, gynecological conditions, infertility, and early puberty. The GnRH analogues are synthetic compounds that are structurally similar to the natural gonadotropin-releasing hormone produced in the body. High levels of gonadotropin-releasing hormone, known as hypergonadotropic states, are considered rare. Consequently, a single measurement may not capture the dynamic changes in the secretion of this hormone. In collaboration with testosterone inside the testes, which is triggered by LH, FSH also sustains sperm production. Progesterone production then decreases and the next menstrual cycle begins — you get your period — when FSH levels start to rise again. As the follicles increase in size, they begin to release estrogen and a low level of progesterone into your blood. This hormone is responsible for physical changes of puberty, like breast development and menstruation. In females, FSH and LH trigger their ovaries to begin producing estrogen. Prolactin appears to act directly on GnRH secreting neurons to block either synthesis or secretion of GnRH. GnRH secreted in a pulsatile manner by neurons with cell bodies in the hypothalamus.GnRH stimulates synthesis and glycosylation of beta subunits of FSH and LH. Testosterone from the testes also exerts negative feedback effects on FSH and LH production by negatively modulating production of GnRH in the hypothalamus. GnRH secreted in a pulsatile manner by neurons with cell bodies in the hypothalamus. Regulation of the hypothalamic pituitary unit is a complex process involving negative feedback mechanisms in the male. As with many hormones, GnRH has been called by various names in the medical literature over the decades since its existence was first inferred. An elevation of GnRH raises males' testosterone capacity beyond a male's natural testosterone level. Lower-than-normal FSH levels usually lead to incomplete development during puberty. For children, higher levels of FSH and LH than expected based on age — in addition to the development of secondary sexual characteristics — are an indication of precocious (early) puberty. In very rare cases, issues with the pituitary gland in females can raise FSH levels. Most often, higher-than-normal levels of follicle-stimulating hormone (FSH) are a sign of an issue in the ovaries or testes (gonads). When dopamine signaling is reduced, the wanting aspect of sexuality fades even when the physical capacity to function remains intact. Some men are sensitive to estrogen shifts in ways that affect mood, arousal, and desire. It originates in the brain, shaped by neurotransmitter tone, emotional context, relationship quality, circadian signals, and neuroendocrine inputs, of which testosterone is only one. Kisspeptin-mediated signaling in the hypothalamus appears to have its own role in generating that central desire, and TRT does not replicate or restore that upstream activity. It may mean the very neural circuits that generate sexual desire are receiving a muted or altered signal. The testes, no longer receiving the LH signal they depend on, reduce their own natural testosterone output and can decrease in size over time. LH and FSH drop, sometimes to very low levels. Selective serotonin reuptake inhibitors, or SSRIs, are among the most commonly used medications in adults and are well-documented to reduce sexual desire, arousal, and orgasmic function in a significant percentage of users. Cortisol, the primary stress hormone, has a documented suppressive effect on kisspeptin neurons and GnRH activity. Elevated prolactin, whether from a small benign pituitary growth, chronic stress, certain medications, or other causes, is a known libido suppressor that operates partly by dampening dopamine tone. There is also the question of what happens to testosterone once it is in the body. A man with suppressed kisspeptin and LH signaling may have adequate testosterone circulating in his blood while still experiencing the equivalent of a dimmer switch turned low on central desire circuitry. It does not release enough GnRH (gonadotropin-releasing hormone), so the pituitary never triggers testosterone or estrogen production. These gonadotropins are the luteinising hormone and the follicle-stimulating hormone, which stimulate the production of sex hormones such as testosterone. These hormones (gonadotropins) stimulate the production of testosterone, estrogen and progesterone. Your body’s production of gonadotropin-releasing hormone (GnRH) affects your sex hormone levels, libido and fertility. Besides secretion, the social environment as well as their behavior affects the size of GnRH neurons. GnRH is found in organs outside of the hypothalamus and pituitary, and its role in other life processes is poorly understood. It has been reported that there are kisspeptin-producing neurons that also express estrogen receptor alpha.
