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Penis development in womb requires more than testosterone

Development of the fetal penis requires not only testosterone from the testes, but a second hormone produced by other tissues, including the placenta, according to a study published in PLOS Biology. The results reveal a previously unknown pathway of masculinisation of the external genitalia, and may explain why placental dysfunction is associated with disorders of male genital development. Testosterone released by the testes of the male fetus is converted to 5α‐dihydrotestosterone (DHT) by the genital tubercle, helping to ensure that this primordial structure develops into a penis rather than a clitoris. Penis development was recently shown to also depend on a second process, the alternative or backdoor pathway, which leads to DHT production independent of testicular testosterone. However, the details of this pathway, including the source of the DHT precursor, have been unclear. Researchers therefore measured levels of different steroids in fetal plasma and tissue during the second trimester, the period of the most critical steps in penis development. They also analysed levels of gene expression for key enzymes in hormone synthesis. They found that androsterone, a precursor of DHT in the backdoor pathway, was the principal circulating androgen in male fetuses, and that circulating levels of both androsterone and testosterone were lower in female fetuses. The investigators also found that the enzymes of the backdoor pathway were primarily located in non‐gonadal tissue, including the liver and placenta. As androsterone can be synthesised from progesterone, the authors suggested that placental progesterone or related compounds may be the precursors of androsterone in the backdoor pathway. While the reasons for the sex difference in fetal androsterone levels are unclear, expression of enzymes that convert androsterone to DHT was found to be high in the male genital tubercle, which thus appears able to produce DHT from both testosterone and androsterone.

https://journals.plos.org/plosbiology/article?id=10.1371/journal.pbio.3000002

Treating insomnia improves back pain

A new systematic review and meta‐analysis from the University of Sydney, published in Osteoarthritis and Cartilage, indicates that treating insomnia can help reduce back pain, further highlighting the complex link between sleep and pain. Chronic low back pain is the leading cause of disability worldwide, affecting an estimated 540 million people at any one time. More than 59% of affected patients also experience insomnia. The researchers analysed data from 24 randomised controlled clinical trials of therapies for sleep disorders in more than 1550 people with osteoarthritis and back or neck pain. In people with back pain, interventions for relieving insomnia, including cognitive behavioural therapy and medication, improved sleep by 33% and reduced pain by 14% compared with control treatments. Based on the study results, the researchers advise that health professionals treating patients with back pain should be conscious of screening for insomnia and referring them for management. While low back pain improved with treatments for insomnia, participants with knee osteoarthritis did not experience major reductions in pain, despite minor improvements in sleep. The researchers’ next step is to conduct studies of combined treatments. They are also exploring the effectiveness of a fully online cognitive behavioural therapy sleep treatment for people with low back pain and insomnia.

https://www.sciencedirect.com/science/article/pii/S1063458418315012?via%3Dihub