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The facts of (modern) life

Male fertility isn't what it used to be: sperm counts have halved in 50 years and disorders of the reproductive system are on the increase. What's causing the 'feminisation' of men? Steve Connor reports

Wednesday 04 February 2004 01:00 GMT
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In 1991, a Danish scientist presented the results of a study to a World Health Organisation conference, showing that the sperm counts of Western men had fallen by about a half over the previous 50 years. Professor Niels Skakkebaek of the University of Copenhagen could offer no explanation for the findings, but neither could he dismiss them as a mere statistical fluke. More than a decade later, scientists are still trying to explain the apparent feminisation of modern man.

There is now mounting evidence that something quite serious is happening to male fertility, and not just in sperm counts. It encompasses a range of disorders of the male reproductive system, and medical researchers have even coined a name for it - testicular dysgenesis syndrome.

The syndrome is a collection of disorders that manifest themselves at one of two stages in life. At birth, it appears as cryptorchidism - the incomplete descent of the one testis or both testes into the scrotum - or a disorder of the penis in which the opening does not develop at the tip, a disfigurement called hypospadia. Later in life, after adolescence, testicular dysgenesis syndrome can appear as more generalised disorders such as low sperm counts, infertility, or cancer of the testes.

There is ample data to suggest that these disorders are on the increase. Cryptorchidism is the most common congenital malformation in children of either sex, affecting between 2 and 4 per cent of baby boys, and hypospadias are the second most common congenital malformation in children. Low sperm counts now affect up to one in five young men, and testicular cancer is the most common cancer of young men, and its incidence has increased steadily over the past 60 years. In fact, were it not for the fact that testicular cancer is so curable, it would be the biggest killer of young men after road-traffic accidents, according to Dr Richard Sharpe, a male-fertility specialist at the Medical Research Council's Human Reproductive Sciences Unit in Edinburgh.

Sharpe is one of several experts in the field who believe that there could be a common basis for all these different problems of the male reproductive system. He 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 of the Centre for Ecology and Hydrology, Windermere. "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."

Most work has centred on the rise of hermaphrodite fish in British rivers, which seems to have happened as a result of the increase in natural and synthetic oestrogens pouring into the aquatic environment from sewage effluent. "Most of the effects seem to be occurring in the aquatic environment. We're not sure why. It might be due to not enough work being done in the terrestrial environment, but I think it is a genuine effect and something do to with the exposure of water-breathers," says Matthiessen.

The contraceptive pill being flushed down the toilet is one obvious reason for the increase in oestrogens in the environment. Natural oestrogens break down relatively easily, but synthetic oestrogens are designed to withstand the rigours of the human intestine - the same traits that prevent them from being broken down by microbes in sewage-treatment works.

The crucial question is whether this environmental chemical, or any others suspected of being endocrine disrupters, are actually getting back into the human food chain to affect foetal development in pregnant women.

Richard Sharpe is keen to assert the importance of not jumping to conclusions. "I'm concerned that people run away and say that because we are investigating something, and because it can cause a similar disorder in animals, then it must cause it in humans," he says. It is in everyone's interest to focus on the disorder rather than on the potential culprits, he says. "If we assume guilt, the real culprit may be able to carry on causing harm while we get side-tracked."

Although scientists have made great strides in understanding endocrine disruption since Professor Skakkebaek's sperm-count study was first brought to the public's attention in 1991, they have still a long way to go before they can explain what is actually happening to the fertility of the human male.

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