A man’s mother is now believed to be at the root of the declining sperm counts in the male population.
It was in 1991 that a Danish scientist first alerted the world to the fact that Western men were suffering an infertility crisis. Professor Niels Skakkebaek of the University of Copenhagen presented data indicating sperm counts had fallen by about a half over the past 50 years. Sperm counts in the 1940s were typically well above 100m sperm cells per millilitre, but Professor Skakkebaek found they have dropped to an average of about 60m per ml. The world was shocked and for the past 20 years scientists have been debating the cause for this radical decline in the male sperm count.
Scientists wanted to know what was causing it, because the changes were occurring too quickly to be a result of genetics. It must have something to with changing lifestyles or the environment of men, and almost everything was suggested, from exposure to chemical pollutants to the modern fashion for tight underpants.
There is now an emerging consensus among some experts that whatever it is that is exacerbating the problems of male infertility, it probably starts in the womb. It is not the lifestyle of men that is problem, but that of their mothers.
The process of sperm production, called spermatogenesis, starts in adolescence, but the groundwork is laid down in the few months before and immediately after birth. An increasing number of studies point to a crucial “window” of testicular development that begins in the growing foetus and ends in the first six months of life. Interfere with this critical developmental period, and a baby boy will suffer the lifetime consequences of being a suboptimally fertile man.
A number of studies point to a connection between early development in the womb and male reproductive problems in later life, especially low sperm counts. For example, men whose pregnant mothers were exposed to high levels of toxic dioxins as a result of the 1976 industrial accident in Seveso, Italy have been found to have lower-than-average sperm counts. But men exposed to dioxins in adulthood showed no such effect. Another study found women who ate large amounts of beef during pregnancy, a diet rich in potentially damaging chemicals called polycyclic aromatic hydrocarbons (PAHs), had sons with relatively low sperm counts. But eating beef as an adult man shows no similar impact.
One of the strongest pieces of evidence in support of this idea comes from studies of people who smoke. A man who smokes typically reduces his sperm count by a modest 15 per cent or so, which is probably reversible if he quits. However, a man whose mother smoked during pregnancy has a fairly dramatic decrease in sperm counts of up to 40 per cent – which also tends to be irreversible.
Such findings can be explained by understanding how the first cells of the testes form. Sertoli cells, which in the adult act as guardians for the development of sperm cells, are the very first cells to form from a “genital ridge” of the human male foetus. The number of sperm that can be produced in an adult man is critically dependent on the number of Sertoli cells that develop in his foetus, so anything that interferes with the formation of Sertoli cells in a mother’s womb will affect sperm production many years later. “Maternal-lifestyle factors in pregnancy can have quite substantial effects on sperm counts in sons in adulthood, and the most logical mechanism by which this could occur is via reducing the number of Sertoli cells,” says Professor Richard Sharpe, a fertility research expert at Britain’s Medical Research Council.
The key now is to identify the relevant lifestyle and environmental factors. This is proving tricky. Obesity, for instance, is a growing problem and it has been linked with reproductive problems in both men and women. One study has also indicated that overweight pregnant women tend to produce sons with poor semen quality. But is it being fat that is the cause, or the environmental chemicals stored in fat?
There has been a lot of interest in chemicals in the environment, especially those that can either mimic female sex hormones – oestrogenic chemicals – or block male sex hormones, specifically testosterone which plays a critical role in stimulating the development of Sertoli cells in the womb. So far, the Seveso study provides the clearest link between human foetal development, low sperm counts and prenatal exposure to an environmental chemical. But the dioxin concentrations from this industrial accident were exceptionally high.
It is more difficult trying to establish a similar, significant link between male reproductive problems and exposure to low concentrations of the many other environmental chemicals that may have weak oestrogenic or androgen-blocking properties, including substances as wide-ranging as pesticides, traffic fumes, plastics and even soya beans. Professor Sharpe says that much of the evidence to date is weak or non-existent.
“Public concern about the adverse effects of environmental chemicals on spermatogenesis in adult men are, in general, not supported by the available data for humans. Where adverse effects of environmental chemicals have been shown, they are usually in an occupational setting rather than applying to the general population,” he says.
So although scientists are closing in on the critical window of foetal development in the womb that determines a man’s fertility status in later life, they are still not sure about what it is that could be affecting this change in his reproductive status. But one thing is clear, it is his mother who almost certainly holds the key.
