TESTICULAR INTERSTITIAL CELLS (LEYDIG CELLS)
animal tissue
MECHANISM CLAIMED
Steinach claimed that obstruction of the vas deferens caused atrophy of the sperm-producing seminiferous tubules while causing compensatory hypertrophy of the interstitial cells (which he called the 'puberty gland'), shifting the testis toward increased secretion of a rejuvenating hormone. This was expected to reverse measurable signs of senescence in men.
MECHANISM ACTUAL
Modern endocrinology identifies the interstitial cells (Leydig cells) as the primary source of testosterone in males. However, vasoligation does not reliably increase Leydig cell secretion or circulating testosterone in humans. The proposed back-pressure mechanism does not produce sustained interstitial hypertrophy in human tissue, and no controlled human studies demonstrated the hormone-shift Steinach predicted. Testosterone was chemically isolated in 1935; synthetic androgens then displaced the theoretical basis for the procedure.
INTERVENTIONS USING IT
NOTES
Testicular interstitial cells (Leydig cells) produce testosterone under stimulation from luteinizing hormone (LH). Steinach incorrectly conceptualized them as a discrete “puberty gland” separable in function from the seminiferous germinal epithelium, and hypothesized that surgically suppressing sperm production would redirect the testis’s secretory output toward this “puberty gland” function. The ingredient in this case is not a substance that was extracted or administered, but rather the cell population that vasoligation was intended to stimulate in situ. The broader biological-substance-transfer lineage connects Steinach’s in-situ Leydig-cell hypothesis to Brown-Sequard’s injectable testicular extracts (1889) and Voronoff’s xenografted tissue (1920): all three proposed that male gonadal secretions could reverse senescence, and all three rested on surrogate endpoints without controlled hard-outcome data.