Testosterone can make you taller, but only if your growth plates are still open. Once those plates fuse, which happens for most males between ages 15 and 17, no amount of testosterone will add height. The relationship between testosterone and height is more complicated than it seems, because the same hormone that drives your growth spurt during puberty is also what eventually stops you from growing.
How Testosterone Drives the Growth Spurt
During puberty, rising testosterone levels are the primary trigger for the male growth spurt. Research measuring 24-hour hormone levels in boys found that the growth spurt correlates directly with increasing testosterone production, not with changes in growth hormone as was once assumed. Testosterone acts on the growth plates (the soft cartilage zones near the ends of your long bones) and stimulates them to produce new bone tissue, making bones longer.
Testosterone does this partly through a growth-hormone-independent mechanism. Animal studies show that testosterone directly widens the active zone of the growth plate and increases the number of receptors for a key growth-signaling molecule called IGF-1. This makes the growth plate more responsive to growth signals. The effect is dose-dependent: higher testosterone levels produce more growth plate activity, at least in the short term.
Why Testosterone Also Stops Growth
Here’s the paradox. Your body converts a portion of testosterone into estrogen through an enzyme called aromatase. That estrogen is what ultimately causes your growth plates to harden and fuse shut permanently. Once fused, bones can no longer lengthen, and your adult height is set.
The clearest proof comes from rare cases of people born without functioning aromatase. Because their bodies can’t convert testosterone to estrogen, their growth plates never close. These individuals keep growing well into adulthood, developing unusually tall stature with disproportionately long limbs. When they receive estrogen treatment, their growth plates close quickly and longitudinal growth stops. This confirms that estrogen, not testosterone itself, is the signal that ends bone growth.
The same principle explains a historical observation: males who were castrated before puberty (losing their testosterone source) developed unusually tall, long-limbed frames. Without testosterone being converted to estrogen, their growth plates stayed open far longer than normal. The earlier the testosterone was removed, the more growth plates were affected, and the taller the individual became.
Testosterone for Delayed Puberty
The most common medical scenario where testosterone is used to influence height involves boys with constitutional delay of growth and puberty (CDGP), a condition where puberty simply starts late. These boys are often significantly shorter than their peers, which can cause real psychological distress.
Doctors sometimes prescribe low-dose testosterone injections to jump-start puberty in these cases. A study comparing different doses found that boys given 50 mg per month achieved their full predicted adult height without any compromise. Boys given 200 mg per month grew faster initially but then decelerated sharply, ending up significantly shorter than their predicted height. The control group, who received no treatment at all, also reached their predicted height but had to wait longer to get there.
The takeaway is important: low-dose testosterone in this context doesn’t make boys taller than they would have been naturally. It accelerates the timeline so they reach their genetic height potential sooner rather than later. High doses, on the other hand, can permanently cost height by advancing bone maturation too quickly.
What Happens if You Take Testosterone While Still Growing
If a teenager or young person with open growth plates takes testosterone without medical supervision, the risk of stunting final height is real. Excess testosterone converts to estrogen faster, which accelerates growth plate fusion. You might see a temporary burst of growth followed by early closure, locking in a shorter adult height than you would have reached naturally.
This is why clinicians use bone age X-rays before prescribing testosterone to adolescents. A bone age X-ray of the hand and wrist reveals how mature the growth plates are, which helps predict how much growth remains. If the bone age is significantly delayed (more than two years behind chronological age), height predictions become less reliable, and doctors use specialized methods to avoid overestimating future growth. The goal is always to confirm that treatment won’t sacrifice final height.
Can Testosterone Add Height in Adults?
No. Once your growth plates have fused, testosterone has no mechanism to lengthen bones. This applies to prescription testosterone therapy, anabolic steroids, and over-the-counter “testosterone booster” supplements. Growth plates are assessed as fused when an X-ray shows complete closure, growth velocity has dropped below 1 cm per year, and secondary sexual characteristics are fully developed. For most males, all three criteria are met by the late teens.
Testosterone therapy in adults affects muscle mass, fat distribution, bone density, and many other systems, but height is not one of them. No supplement or hormone can reopen fused growth plates.
The Window That Matters
The only scenario where testosterone can meaningfully influence height is during a narrow developmental window: after puberty has begun (or should have begun) but before the growth plates close. For boys with delayed puberty, carefully dosed testosterone under medical guidance can help them reach their genetic height potential on a normal timeline. Outside of that specific situation, testosterone either has no effect on height or, if misused during adolescence, can reduce it. The dose and timing make all the difference between reaching your full height and permanently losing inches.