Research in rats has found that penis length is pre-determined by the action of hormones during a limited time frame early in fetal development. Exposure to hormones after this time can speed-up penis growth, but ultimately cannot increase the size reached in adulthood. The research has important implications for clinical management of children born with penile abnormalities. The results are published in the International Journal of Andrology.

The discovery was made by scientists at the Medical Research Council Human Reproductive Sciences Unit at the University of Edinburgh as part of an ongoing programme of research into the origins of common male reproductive disorders.

It builds on early work by Dr Michelle Welsh and Professor Richard Sharpe that has highlighted the importance of action of the hormone androgen during what is described as a ‘masculinisation programming window’ (MPW). When rat and human gestation times are compared, the MPW corresponds to approximately 8 to 12 weeks in human pregnancy. The level of androgen activity during the MPW also determines the distance between the base of the penis and the anus (anogenital distance) making this measurement a life-long gauge of androgen exposure in the womb during the critical MPW.

This most recent research demonstrates that maximal growth potential of the penis is pre-determined by androgen action during the MPW. Because the anogenital distance gives an insight into hormone exposure during foetal development it may be possible to use this measurement at birth to predict future reproductive problems or abnormal adult penis size.

The hormone androgen is required to drive penis growth during foetal development in pregnancy and then later throughout puberty in both humans and in rats. This similarity makes the rat a useful model of disorders that affect the male reproductive system including micropenis (an abnormally small penis), hypospadias (the urinary tract opens in the wrong place on the penis) and some forms of cancer and infertility.

By blocking exposure to androgens during the MPW in rats, the team found that adult penis size was reduced and that exposure to the hormone later in life had no ‘repair’ effect.

Androgen treatment in rats before adulthood did cause premature growth of the penis towards adult size but did not make it larger than the size pre-determined by hormone exposure in the womb.

Lead author Dr Michelle Welsh of the MRC Human Reproductive Sciences Unit said:

‘‘These results highlight that penis development is just like the rest of the male reproductive system in that there are two critical phases, both of which are dependent on androgens. Phase one, penis formation, occurs early in fetal life and is the more important phase, as any deficits in androgen action here cannot be repaired by androgens later in life. Phase 2, penis growth, offers a wider time window for androgen action, anytime from birth to completion of puberty.  Our results provide new understanding of these processes and their timings, which will allow better insight and diagnosis for boys born with mild or severe genital problems.’’

Key facts

Disorders of penis development, especially hypospadias (the urinary tract opening in the wrong place on the penis), are surprisingly common. Data from the US suggest that these disorders are most common in Caucasian boys and have increased by almost 20%, from 0.7% to 0.83% incidence in the population between 1990 and 2000.

In the US Hypospadias occurs in 0.4% of boys at birth. Figures vary around the world, for example in Denmark 1% of boys are born with the condition.

Penis length in normal young adult males is extremely variable (reported to range from 4 - 12.5 cm flaccid length in young males, Ponchietti et al, 2001). Findings reported in this paper could provide an explanation for some of this variation.

Original research paper: Critical androgen-sensitive periods of rat penis and clitoris development, Welsh et al is published in the International Journal of Andrology.

Contact: Press Office, 020 7637 6011, press.office@headoffice.mrc.ac.uk

Source: Medical Research Council