Stunted Growth

Anabolic/androgenic steroids may inhibit linear growth when administered before physical maturity. These hormones actually can have a dichotomous influence on linear height. On one hand, their anabolic effects may increase the retention of calcium in the bones, facilitating linear growth. A number of anabolic steroid programs have been successful in helping children with short stature achieve a faster rate of growth. At the same time, however, anabolic/androgenic steroid use may cause premature closure of the growth plates, which inhibits further linear growth. There have been a number of cases of noticeably stunted growth (short stature) in juvenile athletes that have taken these drugs. The specific outcome of steroid therapy depends on the type and dose of drug administered, the age in which it is administered, the length it is taken, and the responsiveness of the patient.

While androgens, estrogens, and glucocorticoids all inherently participate in bone maturity, estrogen is regarded as the primary inhibitor of linear growth in both men and women. Women are shorter on average than men, and also tend to stop growing at a slightly earlier age, due to the effects of this hormone. Anabolic/androgenic steroids that either convert to estrogen or are inherently estrogenic are, likewise, more likely to inhibit linear growth than other agents. Popular anabolic/androgenic steroids with estrogenic activity include (but are not limited to) boldenone, testosterone, methyltestosterone, methandrostenolone, nandrolone, and oxymetholone. These drugs must be used with additional caution in young patients due to their stronger potential for inducing growth arrest.

Estrogen acts directly on the epiphyseal growth plates to inhibit linear growth. These plates are located at the end of growing bones, and contain a collection of stem-like cells called chondrocytes. These cells proliferate and differentiate to form new bone cells, slowly expanding the length of the bones and the height of the individual. These cells have a finite life span, with programmed senescence (cell death). This will cause the rate of chondrocyte span, with programmed senescence (cell death). This will cause the rate of chondrocyte proliferation to slow over time, and eventually stop. The chondrocytes are replaced with blood and bone cells at the point of physical maturity, “fusing” the bones and inhibiting further linear growth. The stimulation of estrogen appears to accelerate bone age advancement by exhausting the proliferative potential of chondrocytes at an earlier time.

Age will also influence a patient’s sensitivity to epiphyseal fusion. As young children are far from the point of bone maturity, the inhibitive effects of hormone therapy take longer to manifest in growth cessation. As the juvenile ages, they may become more sensitive to these effects. Studies treating teenage boys (average age 14 years) for tall stature, for example, found that six months of testosterone enanthate (500 mg every two weeks) was sufficient to reduce final height by almost three inches compared to the predicted outcome. This is a moderately supratherapeutic dose, underlining the fact that steroid intake during adolescence can have a very tangible impact on height. This issue may not be as simple as avoiding estrogenic steroids either, as non-estrogenic steroids have also induced skeletal maturation. Individuals remain warned of the potential for growth interruption when anabolic/androgenic steroids are used before physical maturity.


Wlliam Llewellyn (2011) - Anabolics

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