Linear growth, which determines a person’s final height, is a biological process that takes place during childhood and adolescence. It is governed by genetics and the regulatory effects of various hormones. Seeking to limit this growth involves intervening in a naturally occurring sequence of skeletal development. The methods available are few and are generally only considered in cases of extreme predicted tall stature or specific medical conditions.
The Natural Timeline for Growth Cessation
The mechanism responsible for increasing height is the epiphyseal plate, or growth plate, a layer of cartilage near the ends of long bones. Cells within this plate continuously divide, enlarge, and are replaced by bone, lengthening the bone. This elongation continues until late adolescence when a biological signal initiates its permanent cessation.
The signal for growth plates to stop functioning comes from the dramatic increase in sex hormones—estrogen and testosterone—that occurs during puberty. These hormones accelerate growth plate senescence, the natural aging and decline of the cartilage cells. Estrogen has a profound effect, regardless of biological sex, by exhausting the pool of progenitor cells responsible for creating new cartilage.
As puberty concludes, the growth plates completely ossify, meaning the cartilage is permanently replaced by solid bone. This event is called epiphyseal fusion or growth plate closure. Once closure occurs, no further increase in height from the long bones is possible. For females, fusion typically occurs around age 16, while for males, it may continue until around age 19, marking the completion of skeletal maturation.
Debunking Common Myths About Height Reduction
Once the growth plates have fused, no non-medical intervention can reduce or halt final adult height. Attempts to influence stature through lifestyle changes, such as specific diets or exercise routines, are ineffective after skeletal maturity is reached. While extreme calorie restriction during childhood can stunt growth, typical adult dieting cannot reverse the height already achieved.
A common misconception is that heavy weightlifting or intense exercise during adolescence can prematurely stop growth, but this is not scientifically supported. While injury to an open growth plate can cause premature fusion, routine physical activity and strength training do not interfere with the normal growth process. Posture changes can make a person appear slightly taller or shorter, but they do not alter the actual length of the bones.
Medical Procedures to Halt Linear Growth
For individuals predicted to reach an extreme height, such as those with constitutional tall stature or certain genetic syndromes, medical interventions are available. These must be performed before natural growth plate fusion. These methods are designed to accelerate or physically force the closure of the growth plates in the legs, reducing the final adult height. The two approaches are surgical intervention and high-dose hormonal therapy.
Surgical Intervention (Epiphysiodesis)
Epiphysiodesis is a surgical procedure that permanently stops the growth plate from functioning. It involves physically damaging or surgically fusing the growth plate cartilage in the long bones, most commonly the distal femur (thigh bone) and proximal tibia (shin bone). Arresting growth in these areas reduces the final length of the legs.
This intervention must be timed precisely to achieve the desired height reduction, requiring surgeons to calculate the remaining growth based on bone age and growth curves. The procedure can be performed using a minimally invasive technique, such as drilling the growth plate or placing screws across it. Potential complications include the development of angular deformities in the limb or the risk of incomplete correction.
Hormonal Treatment
High-dose hormonal therapy is another method used to accelerate the natural closure of the growth plates during adolescence. For biological females, high doses of estrogen were historically administered to speed up growth plate senescence. High estrogen levels mimic the natural hormonal surge of late puberty, causing the growth plates to fuse earlier.
The effectiveness of this hormonal approach depends on the timing of administration; it must be initiated while the growth plates are still open and actively growing. High-dose sex hormones carry significant side effects, including an increased risk of blood clots, ovarian cysts, and other long-term health concerns. Because of these potential risks and the difficulty in precisely predicting the outcome, this method is used less frequently today compared to surgical options.