The question of whether taking testosterone can increase height depends entirely on a person’s stage of skeletal development. Testosterone, the primary androgen and male sex hormone, drives the physical changes associated with puberty, including the growth spurt. However, the hormone’s influence on height is complex, involving two opposing effects. To understand how exogenous (external) testosterone affects final height, one must first understand the finite mechanism that controls linear growth in the human skeleton.
How Height is Determined by Growth Plates
Linear height gain occurs exclusively at structures within the long bones known as the epiphyseal plates, or growth plates. These specialized areas of cartilage are located near the ends of bones, such as the femur and tibia, and act as the “engine” for vertical growth. Throughout childhood and adolescence, cells within the growth plate rapidly divide and expand in a process called endochondral ossification.
This process involves the newly formed cartilage cells gradually calcifying and being replaced by hard bone tissue, which incrementally lengthens the bone. As long as the growth plates remain open, or “active,” the bones can continue to extend, resulting in an increase in height. The final determination of adult stature hinges on the moment this process ceases.
Height growth stops when the hormonal changes of late puberty cause the cartilage in the growth plates to be completely replaced by bone. This event is termed growth plate fusion, or closure, and it typically occurs during late adolescence, generally between the ages of 14 and 19. Once fusion is complete, the bone ends are solidified, and no amount of further cell division or hormonal signaling can restart linear growth.
Testosterone’s Dual Role in Skeletal Development
The influence of natural testosterone on bone development is characterized by a two-phase action that dictates the timing and extent of the pubertal growth spurt. Initially, the rise of endogenous testosterone promotes acceleration in linear growth. This effect is achieved partly through the hormone’s stimulation of the Growth Hormone (GH) and Insulin-like Growth Factor 1 (IGF-1) axis.
Testosterone also acts directly on the growth plates by promoting the proliferation of cartilage cells, leading to a rapid increase in height velocity. However, this growth stimulation is temporary and contains the mechanism that eventually halts it. As testosterone levels remain high throughout puberty, a portion of the hormone is converted into estrogen (estradiol) by an enzyme called aromatase, which is present in various tissues, including the growth plates.
It is primarily this locally converted estrogen that signals the growth plates to slow cartilage production and begin fusion. Therefore, the same surge in testosterone that triggers the rapid growth spurt simultaneously sets the clock for the closure of the growth plates. This narrow window of opportunity is why the timing of any external hormonal intervention is important to final height.
When Exogenous Testosterone Affects Final Height
The effect of exogenous testosterone, such as through prescribed hormone therapy, depends entirely on the status of the individual’s growth plates at the time of administration. For individuals whose growth plates have fused, taking testosterone will have zero effect on increasing linear height. Since the bone structure is solidified, the hormone can only influence non-length-related aspects of bone health, such as increasing bone mineral density.
However, in individuals whose growth plates are still active, the timing of testosterone administration can significantly impact final adult height. If a person with delayed puberty is treated with testosterone, the therapy helps trigger a normal growth spurt, allowing them to reach their genetically predicted height. Without this intervention, they may ultimately fail to reach their full potential.
Conversely, administering testosterone too early in a person whose growth plates are open can be counterproductive to height gain. High doses of testosterone or an early start to therapy can prematurely accelerate the process, causing the growth spurt to be shorter and triggering early growth plate closure. This accelerated skeletal maturation can result in a final adult height that is shorter than what would have been achieved naturally. Medical professionals must monitor bone age to guide therapy, especially in cases of gender-affirming hormone treatment or precocious puberty.