The feminisation of males

An increasing number of baby boys in the UK are being born with genital disorders. One in 350 male babies have a condition known as hypospadias. Instead of the opening of the penis being at the tip, it may be lower down the penis or even around the scrotum. In a few rare cases, there may not be an opening at all.

Other disorders of the male reproductive system are also on the increase. Cryptorchidism is the most common genital malformation of all, when one of both testes fail to descend into the scrotum, affecting between two and four per cent of baby boys. Chordee – a downward curve of the penis, especially when erect – is usually, but not always, associated with hypospadias. Boys with chordee often have to sit down when they relieve themselves. In later life, the severe curvature from chordee can make intercourse impossible.

Many experts believe that the defects seen in male babies are related to a broader problem- the feminisation of men. Male sperm counts have halved since 1941. Infertility and cancer of the testes are also on the rise. Testicular cancer is now the most common cancer in young men. Hypospadias is a congenital (present at birth) anomaly (abnormality), which means that the malformation occurs during foetal development. As the fetus develops, the urethra does not grow to its complete length. Also during fetal development, the foreskin does not develop completely, which typically leaves extra foreskin on the top side of the penis and no foreskin on the underside of the penis.

Professor Richard Sharpe, a male fertility specialist at the Medical Research Council’s University of Edinburgh Centre of Reproductive Health, suggests that all the disorders stem from a problem arising at the key stage in the development of the male foetus during early pregnancy. “From epidemiological studies, we know that each of the disorders is a risk factor for all the others, and that they share several pregnancy-related risk factors,” Sharpe says. “Most importantly, we know that they share hormonal risk factors, in particular, anything that interferes with the production or action of androgens and testosterone [the male sex hormones] during the sexual differentiation process of the foetus that occurs in the womb.”

In other words, the suggestion is that there is something happening early in the development of the male foetus that interferes with the key steps enabling it to develop into a healthy, fertile male. Ever since Professor Skakkebaek made his discovery on sperm counts, environmentalists have suggested that it could be “gender-bending” chemicals – endocrine disrupters – in the environment that are the cause of the gradual feminisation of men. But despite intense research to find these endocrine disrupters, the precise reasons for the problems have not so far been identified.

Some scientists believe that the culprit may just as likely be a change in lifestyle, rather than exposure to some new environmental chemical. John Ashby, from the Syngenta Central Toxicology Laboratory in Macclesfield, says that the focus on an environmental cause may be quite wrong. “The human [reproductive] conditions cannot at the moment be associated with a named chemical,” says Ashby. “There are many lifestyle changes that could be contributing to these conditions, for instance, increased smoking among young women.”

Another possible lifestyle factor that could be playing a role is the significant increase in the intake of dietary fat over the past 50 years. Fat is linked with oestrogens – the female sex hormone – and more fat means more oestrogens, which means a possible increase in the risk of interference with the proper development of male reproductive organs. “The trends on dietary fat are up, and the implications are great for endocrine disruption,” says Ashby.

Nevertheless, work on animals has led to the discovery of some chemicals in the environment that could be playing an important role. Sharpe cites his work on chemicals called phthalates, substances used by industry to soften plastics. He has been able to create a set of disorders in laboratory animals that mimic human testicular dysgenesis syndrome by
exposing pregnant mothers to certain phthalate esters at a key stage of foetal development.

“Phthalates are the most common environmental chemical. They are in the air around us,” says Sharpe. However, he points out, it is too early to jump to the conclusion that this is the cause of the problem. “At present, doses that are 100- to 500-fold higher than the highest reported human exposure are required to induce such effects, and we do not have any proof that phthalates can induce such effects in humans,” he says. “Nevertheless, phthalates are everywhere in our environment, we are all exposed, and the highest exposure appears to be in young women of reproductive age.”

But although the jury is out in terms of what is causing the reproductive problems among humans, the same is not the case for the feminisation documented among wildlife, according to Professor Peter Matthiessen, an independent consultant ecotoxicologist. “People are cautious about saying that there are definite effects on humans, but we have hard evidence for effects on wildlife in all groups, from invertebrates to mammals,” he says. “It’s a real-world issue, not just a theoretical worry. It’s actually happening. The effects range from relatively trivial biochemical changes, probably of no ecological significance, to huge changes in populations and communities of organisms.

Thea Jourdan
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